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THE 



PRACTICE OF MEDICINE 



A GUIDE TO THE NATURE, DISCRIMINATION 
AND MANAGEMENT OF DISEASE 



BY 
A. 0. J. KELLY, A.M., M.D. 



assistant professor of medicine in the university of pennsylvania and assistant 

physician to the university hospital, philadelphia; professor of the theory and 

practice of medicine in the university of vermont; professor of pathology in 

the woman's medical college of pennsylvania ; physician to st. agnes* 

hospital, philadelphia; chief of the pathological department of the 

german hospital, philadelphia; member of the association of 

american physicians and of the interurban clinical 

clob; editor of the American journal of 

the medical sciences. 



ILLUSTRATED 




LEA & FEBIGER 

PHILADELPHIA AND NEW YORK 

1910 






Entered according to Act of Congress, in the year 1910, by 

LEA & FEBIGER, 
in the Office of the Librarian of Congress. All rights reserved. 



©CI.A273UJM 



t ♦ t 



TO MY WIFE 



PREFACE. 



The following pages represent an effort to prepare for the student 
and the junior practitioner of medicine a guide to the nature, discrim- 
ination, and management of disease that should contain the essentials 
unadorned with great detail. Since the determination of what is really 
essential must be a matter of individual judgment, the greatest problem 
encountered w T as what to exclude, so that the book, without exceeding 
a convenient limit, should be comprehensive, properly balanced, and 
in good perspective. An acquaintance with the present development 
and the trend of medical education, and a teacher's appreciation of the 
needs of students, make one realize the embarrassment of riches, the 
large number of facts, too often placed before minds not yet qualified 
to sort them in their order of importance and grasp their mutual bear- 
ings. This defect of medical pedagogy violates the physiology of the 
mind, which is so constituted that the natural stimulus to interest, and 
therefore to recollection, is the tracing of rational connection. The 
resulting mental indigestion and lethargy appear at examination time 
and when the student or junior practitioner is confronted with the 
necessity of applying at the bedside principles ill understood. A book, 
of course, cannot replace actual clinical experience, but it should in 
fairness offer its readers a well-ordered statement of existing knowledge 
as a basis for training their powers of observation and reasoning, espe- 
cially in conformity with opportunities presented at the bedside. 

These considerations determined me to devote most space and atten- 
tion to the practical aspects of medicine; to the elucidation of those 
principles exemplified in disease at the bedside, in hospital wards and 
clinics, and in the consulting room; and to the clinically important and 
more common disorders rather than to the rarer diseases, however 
interesting. Such a plan seemed to offer more of value to students in 
recitations and in hospital-ward and dispensary work, and to practi- 
tioners desiring to recall elusive facts. A systematic arrangement of 
the subject matter has been adopted to facilitate comprehension of the 
mutual relations of different clinical and pathological entities. Empha- 
sis has been laid upon the definition of processes of disease — to impress 
upon the student the necessity of accuracy in his use of terms and in 
his clinical descriptions. Inasmuch as the final object of medicine is 
practice, most space has been devoted to symptomatology, diagnosis, 
and treatment; and to ensure a rational grasp of these main objectives, 
they are presented in their natural relationship by means of brief 



vi PREFACE 

connecting sections on etiological factors, essential anatomical lesions, 
and pathological physiology. The sections on pathological physiology 
might have been considerably expanded; but I venture to hope that, 
although limited to a statement of the main facts, they may prove 
serviceable to students in affording them a broad view of disease and 
of disturbed functions in general. Throughout the book an endeavor 
has been made to portray the nature and natural history of disease, 
to correlate disturbed or perverted function with altered structure, to 
explain the development of symptoms, and to elucidate the sequence 
of cause and effect. Such knowledge is essential to a correct and 
intelligent comprehension and interpretation of morbid phenomena 
(symptomatology and diagnosis), to the ability to forecast and provide 
against contingencies, to judgment of the course, duration, and termina- 
tion of disease (prognosis), and to skill in rational treatment and pro- 
phylaxis. Under the individual diseases, I have, as a rule, emphasized 
at least one method of treatment that I know to be of value from my 
own experience; beyond this point, however, I have depended upon 
the recommendations of acknowledged competent authorities. A 
few formulae have been included as an aid to the junior practitioner; 
these with the other instructions mentioned should serve him in times 
of stress until his experience and judgment warrant his making his 
own modifications. Intentional limitation of space and the primarily 
clinical purpose of the book have made it seem desirable to omit 
discussions of the biological characteristics of the infectious micro- 
organisms and of the technique of laboratory methods of diagnosis. 

A book on such a boundless subject as Medicine must be evolved 
out of the collective experience of the masters of all times and all parts 
of the world, tinctured by the study, investigation, judgment, and 
experience of the author. Although this book, in large part, is based 
upon my own clinical and pathological experience, I must acknowledge 
my indebtedness to the many writers of many tongues whose contribu- 
tions to medicine form the basis of my own knowledge. My experience 
with those disorders known as tropical has been almost limited to the 
rather few imported cases that an active hospital physician encounters 
in a large seaport. I have, nevertheless, included a brief account of 
these diseases, because of the widespread interest recently shown in 
their investigation, and on account of the increasing number of stu- 
dents who purpose practising in our tropical possessions; the clinical 
descriptions, however, are largely a reflection of those of such highly 
esteemed authorities as Manson, Cantlie, Jackson, and others. The 
descriptions of the metazoan parasites have been taken, in many 
instances verbatim, from Stiles — the recognized authority in this 
country. Elsewhere the attentive reader will note my indebtedness 
to other authors — to all of whom, I hope, I have given due credit. 

A. O. J. K. 

Philadelphia, 1910. 



CONTENTS 



SECTION I 

INFECTIOUS DISEASES 

General Observations and Pathological Physiology 17 

BACTERIAL INFECTIONS 

Typhoid Fever 32 

Paratyphoid Fever 60 

Pyogenic Infections 61 

Erysipelas 67 

Pneumococcic Infections 70 

Pneumococcic Infection of the Lung ; Pneumonia . 71 

Meningococcic Infection ; Cerebrospinal Fever 86 

Gonococcic Infection 90 

Tuberculosis 92 

Acute Miliary Tuberculosis 96 

Tuberculosis of the Lymphatic System 100 

Tuberculosis of the Circulatory System 106 

Tuberculosis of the Respiratory System 106 

Tuberculosis of the Digestive System 117 

Tuberculosis of the Genito-urinary System 120 

Tuberculosis of the Nervous System 122 

Tuberculosis of the Bones and Joints 124 

Diphtheria 131 

Influenza ' 143 

Bacillary Dysentery 145 

Tetanus 149 

Cholera 153 

Plague 156 

Glanders 159 

Anthrax 161 

Malta Fever 164 

Leprosy 166 

NON-BACTERIAL FUNGUS INFECTIONS 

Actinomycosis 169 

Mycetoma 170 

Nocardiosis 171 

Pulmonary Aspergillosis 171 

Oidiomycosis 172 

ZOOPARASITE INFECTIONS 

Protozoan Infections 

Amcebiasis 175 

Relapsing Fever 178 

Syphilis '. 180 



viii CONTENTS 

Yaws 193 

Trypanosomiasis ' 194 

Kala-azar 195 

Oriental Sore 196 

Malarial Infections. 197 



Metazoan Infections 

Distomatosis 211 

Pulmonary Distomatosis 211 

Hepatic Distomatosis . 211 

Intestinal Distomatosis 212 

Venal Distomatosis 213 

Teniasis 214 

Intestinal Teniasis ; Tapeworm Infection 214 

Somatic Teniasis 217 

Nemathelminthiasis 218 

Uncinariasis -218 

Strongyloidosis 219 

Ascariasis 219 

Oxyuriasis 220 

Trichocephaliasis 221 

Acanthocephaliasis 221 

Trichinosis 221 

Dracunculosis 223 

Filariasis 223 

Acariasis 224 

Ixodiasis 224 

Sarcoptic Acariasis 224 

Parasitic Insects 225 

Phthiriasis ; Pediculosis 225 

Fleas 225 

Bed-bugs 225 

Myiasis 226 



INFECTIONS OF UNKNOWN OR DOUBTFUL ETIOLOGY 

Variola 226 

Vaccinia 233 

Varicella 235 

Typhus Fever 237 

Scarlet Fever 240 

Measles 247 

Rotheln 250 

Glandular Fever 252 

Rheumatic Fever . . 253 

Pertussis 257 

Infectious Parotitis 260 

Yellow Fever 261 

Dengue 265 

Hydrophobia 266 

Rocky Mountain Spotted Fever 269 

Epidemic Poliomyelitis 270 

Acute Infectious Jaundice 272 

Foot-and-Mouth Disease 273 

Miliary Fever 274 

Milk Sickness 274 

Beriberi 275 

Epidemic Dropsy 277 

Nasha Fever 278 

Japanese River Fever .... 278 

Ponos 279 



CONTENTS ix 

Hill Diarrhoea 280 

Sprue 281 

Epidemic Gangrenous Proctitis 281 

Tropical Phagedena 282 

Tropical Bubo 283 

Ulcerating Granuloma of the Genitals 283 

Verruga 284 

Kubisagari 285 

Gangosa 286 

Ainhum 287 

Goundou 287 

Psittacosis 287 



SECTION II 
INTOXICATIONS 

Alcoholism 289 

Opium Habit \ . . 292 

Cocaine Habit 293 

Lead Poisoning 294 

Arsenical Poisoning 296 

Mercurial Poisoning 297 

Snake-venom Poisoning 298 

Food Poisoning 299 



SECTION III 
DISORDERS OF METABOLISM 

Pathological Physiology 303 

Auto-intoxications 303 

Diabetes . 305 

Diabetes Insipidus 318 

Gout . . 320 

Obesity 327 

Rickets 329 

Scurvy 331 

Amyloidosis 334 

Infantilism . . , . . . . . 335 



SECTION IV 

DISEASES OF THE DUCTLESS GLANDS AND OF 
INTERNAL SECRETION 

Pathological Physiology 337 



CONTENTS 



DISEASES OF THE THYROID GLAND 

Pathological Physiology 339 

Acute Thyroiditis 340 

Goitre 340 

Hyperthyroidism and Exophthalmic Goitre 342 

Hypothyroidism; Cretinism; Myxcedema . . 346 

Tumors and Cysts of the Thyroid 349 

DISEASES OF THE PARATHYROID GLANDS 

Pathological Physiology 349 

Tetany 350 

DISEASES OF THE ADRENALS AND THE CHROMAFFIN SYSTEM 

Pathological Physiology 351 

Addison's Disease 353 



DISEASES OF THE PITUITARY BODY 

Pathological Physiology 355 

Akromegaly 356 



SECTION V 
DISEASES OF THE BLOOD AND HEMOPOIETIC SYSTEM 

Pathological Physiology 359 

Acute Secondary Anemia 365 

Chronic Secondary Anemia 367 

Chlorosis 369 

Pernicious Anemia 373 

Leukemia 378 

Erythremia . , 385 

THE HEMORRHAGIC DISEASES 

Hemorrhage in the Newborn 387 

Purpura 387 

Hemophilia 390 

DISEASES OF THE LYMPH NODES AND LYMPH VESSELS 

Pathological Physiology 393 

Lymphangitis and Lymphadenitis 393 

Lymphangiectasis 395 

Tumors and Tumor-like Formations 397 

Hodgkin's Disease 398 

Diseases of the Thoracic Duct 401 

DISEASES OF THE THYMUS BODY 

Pathological Physiology 402 

Enlargement of the Thymus 403 



CONTENTS xi 



DISEASES OF THE SPLEEN 

Pathological Physiology 405 

Anomalies of Form and Position of the Spleen 406 

Rupture of the Spleen . 406 

Thrombosis, Embolism, and Abscess of the Spleen 406 

Enlargement of the Spleen 407 

Splenomegaly; Splenic Anemia • 407 

Tumors and Cysts of the Spleen 410 



SECTION VI 

DISEASES OF THE CIRCULATORY SYSTEM 

Pathological Physiology 411 

NEUROMUSCULAR DISORDERS OF THE HEART 

Cardiac Pain 415 

Palpitation of the Heart 416 

Arrhythmia 416 

Tachycardia 421 

Bradycardia 422 

DISEASES OF THE MYOCARDIUM 

The Weak or Insufficient Heart 424 

The Overstrained or Irritable Heart 427 

The Fatty Heart 430 

The Infectious Febrile Heart . 431 

The Fibroid Heart ... 434 

Hypertrophy and Dilatation of the Heart 437 

Aneurysm of the Heart 443 

Rupture of the Heart . . 444 

Tumors and Parasites of the Heart 444 

Disease of the Coronary Arteries 444 

DISEASES OF THE ENDOCARDIUM 

Acute Endocarditis 445 

Chronic Endocarditis ... 450 

Chronic Valvular Disease of the Heart 452 

Mitral Insufficiency 455 

Mitral Stenosis 459 

Aortic Insufficiency 462 

Aortic Stenosis 466 

Tricuspid Insufficiency 468 

Tricuspid Stenosis 469 

Pulmonary Insufficiency 470 

Pulmonary Stenosis . 470 

Combined Valvular Lesions 471 

DISEASES OF THE PERICARDIUM 

Pericarditis 478 

Fibrinous Pericarditis 478 



xii CONTENTS 

Serofibrinous Pericarditis 480 

Purulent Pericarditis 483 

Chronic Pericarditis 484 

Hydropericardium 487 

Hemopericardium , 487 

Pneumopericardium; Pyopneumopericardium 488 

Chylopericardium 488 

DISEASES OF THE ARTERIES 

Acute Aortitis 489 

Arteriosclerosis 489 

Angina Pectoris 493 

Aneurysm 497 



SECTION VII 

DISEASES OF THE RESPIRATORY SYSTEM 

Pathological Physiology 505 

DISEASES OF THE NOSE 

Epistaxis 511 

Acute Rhinitis 512 

Chronic Rhinitis 514 

Hay Fever 515 

DISEASES OF THE LARYNX 

Acute Catarrhal Laryngitis 517 

(Edemat ous Laryngitis 519 

Spasmodic L aryngitis 520 

Chronic Laryngitis 521 

Laryngeal Perichondritis 522 

Tumors of the Larynx 523 

DISEASES OF THE TRACHEA AND BRONCHI 

Acute Bronchitis 524 

Chronic Bronchitis 527 

Fibrinous Bronchitis 530 

Bronchiectasis 532 

Bronchial Asthma . 534 

Tracheal and Bronchial Obstruction 537 

DISEASES OF THE LUNGS 

Hemoptysis 539 

Congestion of the Lungs 541 

(Edema of the Lungs 543 

Pulmonary Embolism and Thrombosis 545 

Atelectasis and Collapse of the Lung 547 

Bronchopneumonia . . 549 

Chronic Interstitial Pneumonitis 552 

Pneumonokoniosis . 554 

Emphysema 555 



CONTENTS xiii 

Abscess of the Lung 559 

Gangrene of the Lung 561 

Tumors of the Lung 562 

DISEASES OF THE PLEURA 

Pleuritis 564 

Fibrinous Pleuritis 564 

Serofibrinous Pleuritis 566 

Purulent Pleuritis 574 

Hemorrhagic Pleuritis 576 

Chronic Pleuritis '. 577 

Hydrothorax 579 

Pneumothorax 580 

Chylothorax 583 

Tumors of the Pleura 584 

DISEASES OF THE MEDIASTINUM 

Mediastinitis 584 

Tumors of the Mediastinum 585 



SECTION VIII 

DISEASES OF THE DIGESTIVE SYSTEM 

DISEASES OF THE MOUTH 

Stomatitis 587 

Gangrene of the Cheek; Noma 593 

DISEASES OF THE TONGUE 

Glossitis 594 

Eczema 595 

Leukoplakia 595 

Black Tongue 595 

Macroglossia 596 

Acute (Edema 596 

Ranula 596 



DISEASES OF THE SALIVARY GLANDS 

Ptyalism .596 

Xerostomia 596 

Parotitis . 596 

Gaseous Distention 597 

Calculi 597 

Ludwig's Angina 597 

DISEASES OF THE FAUCES, TONSILS, AND PHARYNX 

Acute Tonsillitis 598 

Chronic Tonsillitis 601 

Pharyngitis 603 

Ulceration of the Pharynx 603 

Acute Infectious Phlegmon of the Pharynx , 604 



xiv CONTENTS 

Retropharyngeal Abscess 604 

Elongation of the Uvula 604 

The Lingual Tonsils 604 

DISEASES OF THE (ESOPHAGUS 

Acute Oesophagitis 605 

Chronic Oesophagitis 605 

Ulceration 605 

Varices 606 

Rupture ....,.*. 606 

Dilatation 606 

Diverticula 606 

Spasm ' 606 

Paralysis 607 

Stenosis 607 

Carcinoma 607 

DISEASES OF THE STOMACH 

Pathological Physiology 608 

Symptomatic Disorders of the Stomach 610 

The Appetite 610 

Thirst 611 

Nausea and Vomiting 612 

Hematemesis 613 

Motor Disorders 614 

Sensory Disorders 616 

Secretory Disorders 618 

Nervous Dyspepsia 621 

Acute Catarrhal Gastritis 622 

Phlegmonous Gastritis 624 

Toxic Gastritis . v 624 

Infectious Gastritis 625 

Chronic Gastritis 626 

Acute Dilatation of the Stomach 629 

Chronic Dilatation of the Stomach 630 

Ulcer of the Stomach and Duodenum 632 

Carcinoma of Stomach 638 

Non-carcinomatous Tumors _ 643 

Hypertrophic Stenosis of the Pylorus 643 

DISEASES OF THE INTESTINE 

Pathological Physiology 643 

Symptomatic Disorders of the Intestine 646 

Motor Disorders 647 

Sensory Disorders . 649 

Secretory Disorders 650 

Intestinal Indigestion 650 

Intestinal Hemorrhage 652 

Mucous Colic 654 

Constipation 655 

Acute Enteritis 657 

Chronic Enteritis 659 

Diarrhceal Disorders of Children 661 

Croupous or Diphtheritic Enteritis 667 

Phlegmonous Enteritis 667 

Appendicitis 668 

Sigmoid Diverticulitis 672 

Ulceration of the Intestine 673 

Intestinal Obstruction , 674 



CONTENTS xv 

Dilatation of the Colon 682 

Infarction of the Mesenteric Vessels 682 

Intestinal Sand 683 

Hemorrhoids 683 

Visceroptosis 685 



DISEASES OF THE LIVER 

Pathological Physiology 687 

Jaundice 689 

Anomalies of Form and Position of the Liver 695 

Diseases of the Bloodvessels of the Liver 696 

Fatty Liver 697 

Acute Yellow Atrophy of the Liver 698 

Active Congestion of the Liver 702 

Passive Congestion of the Liver 703 

Perihepatitis 704 

Acute Perihepatitis 704 

Local Chronic Perihepatitis 705 

General Chronic Perihepatitis 705 

Acute Hepatitis 705 

Acute Non-suppurative Hepatitis 705 

Suppurative Hepatitis 707 

Chronic Interstitial Hepatitis : the Cirrhoses of the Liver . . . . . . 709 

Portal Cirrhosis 710 

Biliary Cirrhosis 717 

Tumors of the Liver 719 



DISEASES OF THE GALL-BLADDER AND BILIARY DUCTS 

Congenital Obliteration of the Biliary Ducts .721 

Acute Catarrhal Cholangitis 722 

Suppurative Cholangitis « 724 

Chronic Catarrhal Cholangitis 725 

Acute Cholecystitis .... 726 

Chronic Cholecystitis 728 

Cholelithiasis 728 

Carcinoma of the Gall-bladder and Biliary Ducts 736 



DISEASES OF THE PANCREAS 

Pathological Physiology 737 

Hemorrhages into the Pancreas . 737 

Acute Pancreatitis 738 

Chronic Pancreatitis 741 

Cysts of the Pancreas 743 

Tumors of the Pancreas 744 

Pancreatic Calculi 745 



DISEASES OF THE PERITONEUM 

Ascites 746 

Acute Peritonitis 748 

Chronic Peritonitis 749 

Multiple Serositis 750 



xvi CONTENTS 

SECTION IX 
DISEASES OF THE URINARY SYSTEM 

Pathological Physiology 755 

Anuria 763 

Albuminuria 764 

Albumosuria 767 

Cylindruria 768 

Hematuria 769 

Pyuria . 769 

Anomalies of Form and Position of the Kidneys 770 

Circulatory Disturbances of the Kidneys 770 

Nephritis 772 

Active Diffuse Nephritis 773 

Acute Suppurative Nephritis 779 

Chronic Diffuse Non-indurative Nephritis 780 

Chronic Diffuse Indurative Nephritis . . 783 

Cystitis; Ureteritis; Pyelitis; Pyelonephritis; Pyelonephrosis 788 

Perinephritis and Paranephritis 792 

Hydronephrosis 793 

Nephrolithiasis 794 

Cysts of the Kidney . 797 

Tumors of the Kidney 798 

Tumors of the Bladder 799 



SECTION X 
DISEASES OF THE NERVOUS SYSTEM 

Pathological Physiology 801 

DISEASES OF THE NERVES 

Neuralgia 808 

Neuritis 811 

Herpes Zoster 813 

Neuromas 814 

Diseases of the Cranial Nerves 814 

Olfactory Nerve 814 

Optic Nerve 815 

Oculomotor Nerve 816 

Trochlear Nerve 816 

Abducens Nerve 816 

Trigeminal Nerve 817 

Facial Nerve 817 

Auditory Nerve 819 

Glossopharyngeal Nerve 819 

Pneumogastric or Vagus Nerve 819 

Spinal Accessory Nerve 820 

Hypoglossal Nerve 820 

Diseases of the Spinal Nerves 821 

Cervical Plexus 821 

Brachial Plexus 821 

Lumbar Plexus 824 

Sacral Plexus . . 824 

Diseases of the Cervical Sympathetic Nerves , , , , . 824 



CONTENTS xvii 



DISEASES OF THE CEREBROSPINAL MENINGES 

Meningeal Hemorrhage 825 

External Pachymeningitis 826 

Internal Pachymeningitis 827 

Leptomeningitis 828 

DISEASES OF THE BRAIN AND SPINAL CORD 

Cerebrospinal Localization 831 

Aphasia 840 

SYSTEM DISEASES OF THE BRAIN AND SPINAL CORD 

Diseases of the Upper (Central) Motor Neuron 

Lateral Sclerosis 845 

Spastic Paralysis of Infants * 846 

Hereditary Spastic Spinal Paralysis 847 

Amaurotic Family Idiocy 847 

Unilateral Ascending and Unilateral Descending Paralysis 848 

Diseases of the Lower (Peripheral) Motor Neuron 

Chronic Anterior Poliomyelitis . . 848 

Progressive Neural Muscular Atrophy 849 

Bulbar Paralysis 850 

Ophthalmoplegia 851 



Disease of the Upper (Central) and the Lower (Peripheral) 

Motor Neurons 

Amyotrophic Lateral Sclerosis 852 



Diseases of the Sensory Neuron 

Tabes Dorsalis 853 

Interstitial Hypertrophic Progressive Neuritis of Childhood 856 

Combined System Diseases 

Hereditary or Family Ataxia 857 

Hereditary or Family Cerebellar Ataxia 857 

Ataxic Paraplegia 858 

Toxic Combined Sclerosis 858 



NON-SYSTEM DISEASE OF THE BRAIN AND SPINAL CORD 

Multiple Sclerosis 859 

DIFFUSE AND FOCAL DISEASES OF THE BRAIN 

Hyperemia of the Brain . 861 

Anemia of the Brain 861 

(Edema of the Brain 862 



xviii CONTENTS 

Cerebral Hemorrhage 862 

Cerebral Thrombosis * 868 

Cerebral Embolism 869 

Thrombosis of the Cerebral Sinuses 870 

Acute Hemorrhagic Encephalitis 871 

Abscess of the Brain 871 

Tumors of the Brain 873 

Hydrocephalus . 875 



DIFFUSE AND FOCAL DISEASES OF THE SPINAL CORD 

Vascular Disorders of the Spinal Cord 876 

Hemorrhage into the Spinal Cord 876 

Caisson Disease 878 

Myelitis 879 

Compression of the Spinal Cord 882 

Tumors of the Spinal Cord 883 

Syringomyelia • 884 



NERVOUS DISEASES OF FUNCTIONAL OR UNKNOWN NATURE 

Migraine 886 

Epilepsy 888 

Hysteria 892 

Neurasthenia and Psychasthenia 895 

Occupation Neuroses 897 

Paralysis Agitans 898 

Acute Chorea 900 

Hereditary Chorea 902 

Convulsive Tics 903 

Choreiform Disorders 904 

Family Periodical Paralysis 904 

Heat Stroke 905 



VASOMOTOR AND TROPHIC DISORDERS 

Angioneurotic (Edema 907 

Erythromelalgia 907 

Acroparesthesia 908 

Raynaud's Disease 908 



SECTION XI 
DISEASES OF THE MUSCLES 

Muscular Rheumatism 911 

Myositis 912 

Progressive Muscular Dystrophy 912 

Myoclonus 914 

Congenital Myotonia 915 

Congenital Amyotonia 916 



CONTENTS xix 

SECTION XII 
DISEASES OF THE BONES AND JOINTS 

Acute Arthritis 917 

Chronic Atrophic Arthritis 918 

Chronic Hypertrophic Osteo-arthritis 920 

Osteomalacia 921 

Osteitis Deformans 922 

Hypertrophic Pulmonary Osteo-arthropathy 923 

Osteogenesis Imperfecta 923 

Achondroplasia 923 

Facial Hemiatrophy 923 

Leontiasis Ossea 924 



THE PRACTICE OF MEDICINE. 



SECTION I. 
INFECTIOUS DISEASES. 



The infectious diseases comprise a series of disorders that result 
from the growth within the living body of divers pathogenic vegetable 
and animal parasites. These, the so-called infectious agents (contagium 
vivum), include certain bacteria, certain non-bacterial fungi, and certain 
zooparasites (protozoa, worms, and arthropods). In consequence, 
one may divide the known infectious diseases into three classes: (1) 
The bacterial infections; (2) the non-bacterial fungus infections; and 
(3) the zooparasite infections; but to these one must at present add 
a fourth class, that of infections of unknown or doubtful etiology — 
which comprise diseases undoubtedly infectious that have not yet 
yielded up to scientific inquiry their specific etiological factors. Perhaps 
the causative agents of many of these, as has been demonstrated of some 
of them (yellow fever, hydrophobia, epidemic poliomyelitis, pleuro- 
pneumonia of cattle, foot-and-mouth disease, etc.), are certain ultra- 
microscopic parasites, microorganisms that pass through a fine porous 
filter impervious to ordinary bacteria, but elude detection by the highest 
powers of the microscope. Additional reasons, however, for the non- 
discovery of these organisms are that they may be difficult to stain, 
difficult or impossible to cultivate in artificial media outside the body, 
and present in small numbers in the diseases they provoke. 

Infectious and Contagious Diseases. — In times past the diseases now 
recognized as infectious were divided into two classes — the miasmatic 
and the contagious. The miasmatic diseases were those surmised to 
be due to some cause, a miasm, arising without the body and capable 
of provoking disease without the intervention of another individual 
thus affected; the contagious diseases were those caused by some 
factor, a contagion, developed within the diseased body and capable 
of transmitting the disease to another individual (man or animal) . either 
directly or indirectly (through the medium of a third person or an 
2 



18 INFECTIOUS DISEASES 

object, or the air). Since a miasm has become a myth of the past, the 
miasmatic diseases have completely disappeared; but the terms con- 
tagious and infectious still obtain. Perhaps a satisfactory distinction 
may be drawn between them: The term infectious diseases is the 
broader, and includes the contagious diseases. The term contagious 
was and still may be used to designate diseases readily transmissible 
from the sick to the well by direct or indirect contact; diseases which 
seem to be transmitted through the medium of the air and in which 
(as in smallpox, measles, scarlatina, etc.) a zone of " contagious atmos- 
phere" seems to surround the patient; and diseases of which the causal 
infectious agent, or contagium vivum, seems to be ill-adapted to lead 
a prolonged existence outside the living body. This distinction, which 
is based upon the ability or lack of ability of the infectious agent to 
lead respectively a parasitic or a saprophytic existence, is largely artificial, 
since borderland cases occur and diseases ordinarily not contagious 
in the aforementioned sense may become so (pneumonia, typhoid 
fever, etc.). The distinction, however, has a practical bearing, in that 
the diseases thus called contagious may be effectually controlled by 
isolation of the patient and strict hygienic precautions, whereas those 
that may be called the non-contagious infectious diseases are not thus 
so readily controlled; but in this respect also borderland cases occur 
(some cases of typhoid fever, pertussis, measles, scarlatina, etc.). The 
terms transmissible and non-transmissible and communicable and non- 
communicable have been proposed to surmount the supposed difficulty 
— which also is largely artificial; the term infectious diseases is a satis- 
factory and all-inclusive term. 

Transmission of the Infectious Diseases. — The records of antiquity, 
as well as of more modern times, definitely prove that many of the 
infectious diseases, notably plague, cholera, dysentery, typhoid fever, 
yellow fever, Malta fever, malaria, influenza, and many so-called 
tropical disorders, have a permanent habitat, are endemic, in certain 
parts of the world. Some of these diseases are seldom or never en- 
countered beyond the confines of their permanent habitat; others, 
from time to time, under various influences, spread from these endemic 
centres to more or less distant regions, or they increase in number and 
perhaps virulence in regions where they prevail continuously — the 
disease becomes epidemic. The epidemic may be local, as in familial, 
house, school, barracks, jail, and town epidemics, or it may be widespread, 
extending throughout several adjoining States or countries; the disease 
even may become pandemic, as has frequently happened in connection 
with plague, cholera, influenza, etc., originating in the Orient. 

The infection may be spread by aerial convection, by contamination 
of the water supply, by infected persons, by a third person, by fomites 
(caravans, cargoes, baggage, rags, money, especially along lines of 
travel and commerce, as well as public drinking vessels, personal cloth- 
ing, bed-linen, room furnishings, table utensils, children's toys, etc.), 
and by domestic animals, rats, mosquitoes, flies, fleas, bedbugs, ticks, 



PATHWAYS OF INFECTION 19 

and other insects. Each of these modes of infection may be active 
under varying circumstances; but from time immemorial special 
importance has been attributed to transmission by means of fomites. 
Unquestionably, fomites are of importance; but since it has been 
definitely proved that malaria and yellow fever are transmitted by the 
bites of mosquitoes, that the personal and bed-linen and even the dis- 
charges of yellow-fever patients are not infectious, and that plague is 
transmitted by means of fleas that infest plague-infected rats, the fomites 
theory has been robbed of much of its former importance; and since 
it also has been definitely proved that many persons convalescent from 
certain infectious diseases, as well as others long since recovered and 
apparently healthy, are unconscious "carriers" of the specific infectious 
agent (typhoid fever, dysentery, diphtheria, scarlatina, meningococcic 
infection, cholera, etc.), the prime importance of direct infection from 
person to person has become more fully realized. The simultaneous 
infection of many persons in a community suggests, as a rule, aerial 
convection of the infectious agent (as in influenza) or contamination 
of the water supply (as in typhoid fever, cholera, dysentery, etc.); but 
many, usually small, but also widespread, epidemics may often be 
traced to a single individual. In prophylaxis, to be presently men- 
tioned, the significance of all modes of infection must be duly appre- 
ciated; but it is unwise to overestimate the significance of fomites, and 
to overlook the slight sore throat (diphtheria), persisting oral and nasal 
discharges (diphtheria and scarlatina), and the chronic carriers of typhoid 
and dysentery bacilli in the stools — all of which are frequently respon- 
sible for more or less serious and widespread, though usually local, 
epidemics. 

Pathways of Infection. — In health, the blood, the viscera, and the 
tissues generally are free from pathogenic bacteria, although the bronchial 
lymph nodes may contain more or less quiescent tubercle bacilli and 
the liver partly disintegrated colon and perhaps other bacilli; but the 
sKin, the nose, mouth, and throat, the intestinal tract, and the female 
genital tract harbor an extensive bacterial flora. This for the most 
part consists of non-pathogenic bacteria, largely organisms of putre- 
faction; but sometimes pathogenic bacteria also are found, leading a 
saprophytic existence — pyococcic on the skin and in the nose, mouth, and 
throat, Bacillus coli, Bacillus pyocyaneus, pyococci, various anaerobic 
bacteria, etc., in the intestinal tract, and so forth. 

Infection of the body with pathogenic bacteria may occur during 
intra-uterine life — so-called congenital or transplacental infection; after 
birth infection may occur by way of the skin, especially through the 
hair follicles, the sebaceous or sweat glands, or abrasions or wounds; 
by way of the respiratory tract, the digestive tract, or the urogenital 
tract; or directly into the blood (direct inoculation, bites of insects, 
etc.). Bacteria that do not succumb in the body are eliminated largely 
through the intestinal and the urinary tracts (feces and urine), but 
some also are eliminated with discharges from the genital tract in women, 



20 INFECTIOUS DISEASES 

by expectoration, coughing, sneezing, etc., and from open, especially 
suppurating, wounds, etc. Outside the body the bacteria may die, 
chiefly under the influence of sunlight, desiccation (absence of suitable 
moisture), inappropriate temperature, and insufficient or inappropriate 
nourishment. Many bacteria, however, live for varying periods, 
especially if they pass into the spore stage, and contaminating the air, 
soil, or water, or attaching themselves to persons, places, or things, 
may subsequently give rise to new infections. 

Nature and Lesions of the Infections. — When exposed to infection, 
the body may be in a receptive or a refractory state, that is, it may 
be susceptible to or immune to the infection. The severity of an ensuing 
infection is determined somewhat by the pathway of infection, but 
largely by the number and virulence or the infecting microorganisms, 
by the presence or absence of associated microorganisms (mixed, 
double, concurrent, or secondary infections), and by the resistance of 
the subject, that is, by a natural or acquired, active or passive, partial 
or complete immunity. This resistance or immunity, which is an 
expression of the phagocytic, antitoxic, and bactericidal properties of 
the blood, is of much importance, and serves to explain the exemption 
from infection of certain individuals exposed thereto. It may become 
reduced under varying circumstances, such as exposure to cold and 
dampness (catching cold), fatigue, improper or insufficient food, hemor- 
rhage, and debilitating diseases like chronic cardiac and pulmonary 
disorders, diabetes, nephritis, malignant disease, etc. In the last-named 
conditions, secondary or terminal infections, due usually to the pyococci, 
Bacillus coli, etc., are common, and are often directly responsible for 
the fatal issue. 

The pathogenic activity of the infectious bacteria is exerted almost 
exclusively through the production of specific poisons. These bacteria, 
therefore, are included with the substances known collectively as antigens 
(antibody generators), that is, organic agents, which, when introduced 
into the body, not only give rise to the presence in the blood serum of 
toxic substances, but also provoke the formation by the cells of the 
body of various antibodies which also pass over into the blood serum. 
These comprise: (1) Pathogenic bacteria; (2) the poisonous secretions 
or products of certain zooparasites (Treponema pallidum, trypanosomes, 
etc.); (3) animal cells, extracts, or fluids (erythrocytes, blood serum, 
snake venom, cells or extracts of different organs, etc.); and (4) vege- 
table cells or extracts (ricin, abrin, etc.). The term toxin is often used to 
include all the poisonous products of bacteria, of which, however, several 
kinds may be distinguished, although they are not always separable the 
one from the other. Of the different toxins and antibodies, the follow- 
ing are the most important: (1) Toxins (extracellular toxins), prod- 
ucts of the secretory (or excretory) activity of the bacteria (especially 
Bacillus diphtherias, Bacillus tetani, the pyococci, etc.). These are 
enzyme-like bodies, separable by filtration from the bacteria, and 
are rendered inactive by heating to 56° C; they exert a destructive 



NATURE AND LESIONS OF THE INFECTIONS 21 

(degenerative) action on the body cells; and they provoke the formation 
in the body of substances that inhibit their action, so-called antitoxins, 
with which they probably unite chemically. Some of these toxins 
have a special affinity for certain tissues — the tetanus toxin, the hydro- 
phobia virus, and the lepra bacillus for the nervous system; the menin- 
gococcus for the meninges; the gonoccocus and its toxin for the serous 
lining of the joints, etc. (2) Endotoxins (intracellular toxins), either 
a part of or intimately bound to the bacteria, and liberated only upon 
lysis or destruction of the bacteria. These also exert a destructive 
(degenerative) action on the body cells; they probably give rise to little 
if any antitoxin formation, but they do provoke the formation in the 
body of bacteriolytic substances. (3) Mycoprotein (bacterial protein), 
the bacterial substance itself, the chief action of which seems to be 
exerted locally — in the production of inflammation and leukocytic in- 
filtration (chemotaxis). (4) Lysins, substances that give rise to solution 
not only of the provoking bacteria, but also of the body cells — whence 
one speaks of bacteriolysins, cytolysins, especially hemolysins, endo- 
theliolysins, hepatolysins, nephrolysins, etc. The lysins of certain 
bacteria have been definitely demonstrated, especially those of the 
staphylococci (staphylolysin), streptococci (streptolysin), Bacillus tetani 
(tetanolysin), Bacillus coli, etc. In infections with these bacteria 
an antilysin is formed, and may be found in the blood serum. For 
the occurrence of an effective lytic action, such as hemolysis, it is 
necessary to have the interaction of an antigen (bacteria, alien erythro- 
cytes, etc.), specific antibodies (so-called immune bodies, or ambo- 
ceptors), and an active complement (completing substance, cytase, 
alexin) which is present in the blood serum of all normal animals. 
The union of the amboceptor and the complement constitute the lysin. 
(5) Agglutinins, substances that give rise to the agglutination or clump- 
ing of the specific infecting microorganism, as well as the agglutination 
or fusion of erythrocytes. The agglutination of pathogenic micro- 
organisms constitutes the so-called Pfeiffer phenomenon, and is utilized 
in the Gruber-Widal reaction, of much diagnostic importance in typhoid 
fever, paratyphoid fever, bacillary dysentery, Malta fever, etc. Agglu- 
tination or fusion of erythrocytes is believed to be the cause of certain 
hyaline thrombi found in typhoid fever and other disorders. (6) Pre- 
cipitins, substances that lead to the precipitation of bacteria, or to 
the formation of a sediment (precipitate) when added to a solution of 
the antigen that provoked their formation. This forms the basis of 
a test serviceable in the recognition of human blood. If a foreign 
protein, such as human blood serum, be injected into a rabbit, the 
rabbit's blood serum is presently found to contain a substance (precipi- 
tin) which, when the rabbit's serum is added to a suspension of some 
human blood (the one-thousandth part of a milligram or less), gives rise 
to a visible precipitate; this phenomenon does not occur if the rabbit's 
serum is added to other than human serum, except that of some of the 
anthropoid apes, and with these the reaction does not occur in such 



22 INFECTIOUS DISEASES 

high dilutions as with human serum. (7) Opsonins, substances that 
so act upon the infecting bacteria that they are readily destroyed by 
the phagocytes. (8) Aggressins, substances that act upon the phagocytes 
and other protecting agencies so as to inhibit or destroy their power of 
protecting the body from infection. In addition to the aforementioned 
predominant toxic influences, bacteria may provoke, usually relatively 
minor lesions, directly by obstructing small capillary or other vascular 
areas (bacterial emboli), or by being present in excessive numbers in 
the circulating blood (anthrax). 

An established infection may be localized, that is, confined to the 
point of inoculation or some other point whence, immediately following 
inoculation, the bacteria are transported, or it may become generalized. 
In some local infections the body generally may be not at all affected, 
although the local lesions may increase somewhat in extent by con- 
tinuity or contiguity of tissue. In other cases, the toxins formed 
locally gain access to the blood stream and the lymph stream and 
occasion a toxemia (bacterial intoxication) and certain general lesions 
and symptoms; this is especially marked in typhoid fever, diphtheria, 
scarlatina, tetanus, pyococcic infections, variola, etc. In still other 
cases the bacteria themselves invade the blood stream or the lymph 
stream, and give rise to a general hematogenous or lymphogenous 
infection (as the case may be), to a so-called bacteremia; this is notably 
the case in typhoid fever, syphilis, glanders, anthrax, many pyococcic 
infections, etc. Although some infections, such as tetanus, diphtheria, 
tuberculosis, etc., are almost if not quite always pure toxemias, and 
others, such as typhoid fever, syphilis, anthrax, etc., are always bac- 
teremias, in the majority of infections no sharp line of demarcation 
can be drawn between toxemias and bacteremias. In most cases, 
as already stated, the lesions and symptoms are due to the bacterial 
intoxication, but bacteremia is much more common than is generally 
supposed; the bacteria, being carried to the different organs of the 
body, set up disseminated foci of disease (so-called bacterial metastases), 
analogous to those of the primary lesion. 

The local and general results of infection vary with the nature of 
the infecting microorganism and its toxin, and with the tissues especially 
involved. In general, the local results consist of toxic degeneration 
of the cells and tissues, which may progress to complete necrosis, and 
of reactive changes comprised within the term inflammation. The 
inflammatory phenomena may be simple and non-specific, and serous, 
serofibrinous, fibrinous, purulent, or hemorrhagic in character, the 
same bacterium under varying circumstances giving rise to varying 
grades of exudation or proliferation; in other cases, the inflammatory 
phenomena may be specific, that is, so characteristic as to enable one 
thereby to postulate the nature of the initiating microorganism (tuber- 
culosis, syphilis, glanders, etc.). In chronic infections there is likely 
to be also considerable formation of new connective or cicatricial tissue. 

The general results of bacterial intoxication vary considerably in 



PATHOLOGICAL PHYSIOLOGY OF THE INFECTIONS 23 

different cases, but the most constant and conspicuous lesions consist 
of parenchymatous and sometimes fatty degeneration of the viscera, 
especially the myocardium, the liver, the kidneys, and the muscles. 
In addition, one may encounter focal necroses of the liver and the 
lymphoid tissues (the lymph nodes, the spleen, and the bone marrow), 
the result of the local action of the toxins or of occlusion of small vascular 
areas by large phagocytic cells or thrombi made up of fused erythro- 
cytes (the consequence of the action of hemagglutinins). The spleen 
often becomes considerably enlarged, due in part at least to hyperplasia 
and multiplication of the endothelial cells of the splenic pulp — which 
cells become phagocytic and are perhaps otherwise concerned in the 
production of immunizing bodies (as in typhoid fever, for instance); 
in part the enlargement of the spleen is due also to the accumulation 
of large numbers of degenerated erythrocytes (the consequence of the 
action of hemolysins). In some cases degenerative changes occur 
in the nerves. In other cases small hemorrhages develop beneath the 
skin or mucous membranes or in the tissues, especially in typhus fever, 
variola, cerebrospinal fever, scarlatina, pyococcic infections, etc.; in 
some of these cases, notably the pyococcic infections (so-called malig- 
nant endocarditis, etc.), the hemorrhage often results from rupture 
of miliary (so-called mycotic) aneurysms, whereas in other cases the 
hemorrhage occurs in consequence of the action of an endotheliolysin 
that destroys the cells of the capillaries and the lining of the small 
arterioles, and thus permits the extravasation of blood. In many 
infections, changes in the composition of the blood are conspicuous, 
notable anemia and leukocytosis; these may be associated with changes 
(usually delay) in the clotting time of the blood and various ill-under- 
stood alterations in the constitution of the plasma. The anemia is 
due at first to increased hemolysis, but later often to interference with 
the erythroblastic function of the bone marrow (defective hemogenesis). 
The leukocytosis is an active process, commonly attributed to chemo- 
taxis, and the result largely of proliferation of the leukoblastic tissues 
of the bone marrow; it is a beneficial process, constituting, together 
with the phagocytic, antitoxic, and bactericidal properties of the blood, 
the process whereby the body becomes protected against or immune 
to infections. Leukocytosis is notably absent in typhoid fever, malaria, 
measles, rotheln, influenza, mumps, the early stages of tuberculosis 
(except the meningeal form), and leprosy. The cause of this is not 
well understood, but it is attributable, in typhoid fever at least, to 
degenerative changes in the bone marrow; in other cases it may be 
due to the absence from the blood serum of a positively chemotactic 
substance. 

Pathological Physiology of the Infections. — The evidence of reaction 
on the part of the body to an established infection, that is, the onset 
of symptoms, may occur soon after the infection has taken place, or 
it may be delayed for a variable, even long, time. It is delayed until 
the toxins are present in such amount and virulence as to overcome 



24 INFECTIOUS DISEASES 

the neutralizing or antagonistic forces of the body, to disturb the func- 
tional activity, and compromise the structural integrity, of the constituent 
cells. This period, that is, the period that intervenes between the 
time the pathogenic microorganisms begin to increase and, multiply 
within the living body and the onset of symptoms, is known as the 
period of incubation. This varies considerably in duration in different 
diseases and somewhat in different cases of the same disease; it may 
be apparently twelve hours or less in some cases of pneumococcic 
infection of the lung (croupous pneumonia), and as much as two to six 
or more months in hydrophobia. In many infections this period is 
unannounced by symptoms; but in some infections, notably typhoid 
fever, toward the end of this period, concurrently with the diffusion 
throughout the body of some toxins or the dissemination of the causa- 
tive bacteria, certain more or less ill-defined, so-called prodromal or 
premonitory, symptoms become manifest, such as malaise, lassitude, 
muscular weakness, and readily induced weariness, general neuro- 
muscular pains and soreness, headache, mental hebetude or irritability, 
perhaps even slight rise of bodily temperature, etc. 

The onset of definite symptoms, the so-called period of invasion, 
may be abrupt (acute) or insidious (subacute or chronic). In certain 
acute infections, such as croupous pneumonia, malaria, etc., the period 
of onset may usually be determined with great exactitude, the invasion 
symptoms consisting of a more or less severe chill and fever. Similar, 
but less aggravated phenomena may attend the onset of other acute 
infections; in infants and children the initial chill or chilliness is often 
replaced by a convulsion. In infections of more insidious development, 
such may be the gradual increment of symptoms that it may be almost 
if not quite impossible to determine accurately the time of onset of 
the disease. In infections generally, of all the symptoms of invasion, 
fever is the most constant and most significant. Such, in point of fact, 
is its significance that in the great majority of cases its occurrence 
should be interpreted to mean infection or intoxication; other less 
common causes comprise the action of enzymes such as are liberated 
during hemolysis (internal hemorrhages, certain severe anemic states, 
burns, etc.), the excessive action of internal secretions (thyroid), grave 
perturbations of the central nervous system associated with increased 
heat production or lessened heat dissipation, exposure to high external 
temperature, and certain drugs (strychnine poisoning, etc.). 

Following upon the period of invasion, the infections are characterized 
by a more or less prolonged period of fever, the so-called fastigium — 
which may last several hours, several days, or several months or more. 
The type and course of the infection may be acute, subacute, or chronic. 
The acute infections, such as measles, scarlatina, smallpox, croupous 
pneumonia, typhoid fever, relapsing fever, etc., are characterized by 
a definite period of incubation, a characteristic, often abrupt period 
of onset, a definite fastigium (typical fever course), and often quite 
characteristic if not pathognomonic symptoms. Depending upon the 



PATHOLOGICAL PHYSIOLOGY OF THE INFECTIONS 25 

virulence of the infectious agent and the resistance of the subject, 
recovery or death eventually occurs. In favorable cases, following 
the fastigium, defervescence ensues — the temperature falls either 
suddenly (crisis) or slowly (lysis), the other symptoms abate, and 
convalescence becomes established. The convalescence, however, 
may be interrupted by relapses or complications (often secondary 
infections), and restoration to complete health may be delayed by 
sequels. Certain of the acute infections are sometimes characterized 
by dominant intoxication, marked mental depression or coma, slight 
fever or even subnormal temperature (that is, little or no reaction), 
rapid and feeble pulse, low and falling blood pressure, absence of 
leukocytosis in diseases in which it ordinarily occurs, and early death. 
These cases are often spoken of as hyperacute, fulminating, or malig- 
nant; they are sometimes exemplified in smallpox, cholera, yellow 
fever, plague, pyococcic (especially streptococcic) infections, cerebro- 
spinal fever, scarlatina, malaria, etc. The chronic infections, such as 
tuberculosis, glanders, actinomycosis, etc., as a rule, are characterized 
by a variable period of incubation, although syphilis is a noteworthy 
exception, having a definite period of incubation; as a rule, also, they 
are insidious in onset, a distinct period of invasion often being undeter- 
minable; and their course is protracted. To intermediate cases the 
term subacute is often applied; other cases, characterized by periods 
of remission and of relapse or exacerbation, are spoken of as remittent 
or recurring. Finally, Adami has postulated what he describes as 
subinfection, a condition in which pathogenic and non-pathogenic 
bacteria, instead of proliferating, are destroyed in the various tissues 
and organs, especially the liver and the mesenteric lymph nodes, to 
which they may be carried by the lymph and blood stream. The long 
continuation of this process is believed by Adami to lead ultimately 
to cell exhaustion and to be perhaps a factor in the production of cirrhosis 
of the liver, some cases of pernicious anemia, some cases of chronic 
interstitial nephritis — an opinion that has not yet found confirmation. 
The obtrusive characteristic of the infections is fever; but increased 
temperature is only one feature of the febrile state. Although under 
the influence of bacterial intoxication the thermogenic regulating 
centres are much disturbed, the increased temperature is due largely, 
if not wholly, to increased heat production, which in turn results from 
augmented tissue katabolism and oxidation; that is, under the influence 
of bacterial toxins, and independently of the amount and character 
of the food, tissue destruction is greater than tissue formation; the 
tissue destruction, however, may be somewhat controlled by appropriate 
food. Adami looks upon fever as the process of adaptation to such 
agencies as can be neutralized by the development of antibodies. Since 
it represents the reaction of the body to the infection, and in an other- 
wise toxic case is to some extent a measure of that reaction, it is by no 
means an unmixed evil; it shows that the body is coping better with 
the infection than if fever did not occur. Although hyperthermia, 



26 INFECTIOUS DISEASES 

especially if prolonged, is of itself dangerous to life, the toxic apyretic 
cases, particularly cases in which the manifestations of intoxication 
increase while the temperature falls, are really serious and commonly 
terminate fatally. 

As already stated, the fever of invasion is often accompanied by a 
more or less severe chill; this is the more likely to occur if the initial 
(pyrogenetic) stage of the fever is short — from one-half to two hours; 
in other cases there may be only chilliness, which may last for some 
time or be repeated. The chill is a nervous manifestation, characterized 
by subjective sensations of coldness, chattering of the teeth, fibrillary 
twitchings of the muscles, and pallor and lividity of the face and ex- 
tremities. Although the patient feels cold and complains thereof, 
the internal temperature of the body is increased. The condition is 
attributable to contraction of the peripheral bloodvessels under the 
influence of vasomotor stimulation, in consequence of which the surface 
of the body is ill-supplied with blood, while the internal organs are 
congested; the fibrillary twitchings and the increased tone (rigor) of 
the muscles are doubtless in part responsible for the augmented heat 
production. 

In addition, the febrile state is characterized by other nervous 
manifestations, as well as disturbances of the circulatory, respiratory, 
digestive, and urinary systems, and disorders of general metabolism. 
The nervous manifestations may be irritative or depressive : the irritative, 
which usually precede the depressive, consist of general neuromuscular 
pains and soreness, headache, mental irritability, intolerance of light 
and noises, insomnia, active delirium, etc.; the depressive consist of 
mental hebetude, apathy, inattention to surroundings, retention of urine 
or involuntary evacuation of the bladder and rectum, muttering delirium, 
stupor, coma, etc. These are attributable to a direct action of toxins 
on the central nervous system, which at first is irritated and finally 
exhausted. In some cases nervous symptoms are unusually dominant 
and give rise to so-called cerebral types of several infections ; these very 
much simulate meningitis, and constitute the so-called meningism of 
the French. In other cases, such as tetanus, hydrophobia, epidemic 
poliomyelitis, etc., the toxin (or virus) possesses a special affinity for 
the nervous system, and may reach the central nervous organs by way 
of the peripheral nerves. 

Rapidity of the cardiac action and of the pulse is an almost constant 
concomitant of the febrile state; as a rule, each degree of added tem- 
perature corresponds to about ten added cardiac beats per minute, 
but there are exceptions: in typhoid fever, for instance, the pulse is 
commonly disproportionately infrequent, in scarlatina it is character- 
istically disproportionately rapid, and in the event of stimulation of the 
pneumogastric nerve (as in meningitis), it may be very infrequent. In 
addition to being rapid, the pulse may be full and bounding, with normal 
or perhaps increased blood pressure (in sthenic states); or weak, easily 
compressible, or thready, with lowered blood pressure (in asthenic 



PATHOLOGICAL PHYSIOLOGY OF THE INFECTIONS 27 

states). Increasing rate and weakness are of bad prognostic omen, 
whereas decreasing rate and increasing strength render the outlook 
hopeful. These changes are the result of various factors: perhaps 
early there is toxic stimulation of the accelerator nerves and increased 
excitability of the heart, and consequent increased pulse rate; later 
toxic degeneration of the myocardium occurs and leads to depression 
of contractility and tonicity and more or less ineffectual systoles; toxic 
degeneration of the pneumogastric nerves may be answerable for some 
of the sudden deaths that occur during the course of or in convalescence 
from diphtheria, influenza, etc.; and toxic paralysis of the vasomotors 
is responsible for the lowered blood pressure and the common capillary 
stasis, especially of the fingers, toes, nose, ears, etc. 

Furthermore, the respiratory rate and the respiratory exchange of 
gases become increased. The increased respirations are due to a direct 
action of the toxins and the augmented temperature on the respiratory 
centres and to surcharging of the blood with carbon dioxide; the in- 
creased gaseous exchange in the lungs is a direct consequence of the 
increased metabolism, of the increased formation of carbon dioxide, 
and the necessity for more oxygen. The increased respirations serve 
in a measure to reduce the bodily temperature, some of which is dis- 
sipated in the process of warming the increased amount of air inhaled. 
The chief digestive disturbances consist of anorexia, dry mouth, thirst, 
lessening of the digestive juices, and often constipation; the gastric 
juice, as a rule, is lessened in amount and reduced in acidity; the bile 
becomes inspissated and is perhaps otherwise altered; the intestinal 
juices are reduced in amount, which together with diminished peristalsis 
is answerable for the constipation of some cases. The urine becomes 
reduced in amount, concentrated, of heightened color, increased acidity, 
increased specific gravity, and increased toxicity; it contains an increased 
amount of nitrogenous substances (urea, uric acid, kreatinine, etc.) 
and of potassium, magnesium, and calcium salts, but sometimes 
there is a decrease of the chlorides; there is often also a small amount 
of albumin, and sometimes hyaline and other casts; in the event of 
intestinal putrefaction, decomposition products, such as indol, skatol, 
and other aromatic substances, may be encountered. The significant 
change from the normal is the great increase in the nitrogenous excretion, 
which may reach twice or thrice that of a normal person on a like diet; 
this is the result of the augmented katabolism affecting especially the 
proteins of the body. One evidence of this is seen in the emaciation 
of the infected subject — at first the panniculus adiposus disappears, 
but the muscles soon decrease in size, lose their tone, and become soft, 
flabby, and readily exhausted. 

The foregoing statements in reference to the bacterial infections apply 
with equal force, although in somewhat modified form, to the non- 
bacterial fungus infections and the zooparasite infections. Some of 
the protozoan infections, such as malaria, syphilis, relapsing fever, 
trypanosomiasis, etc., exhibit many analogies with bacterial infections — 



28 INFECTIOUS DISEASES 

the fever, toxemia, hemolysis, disturbances of metabolism, etc. Some 
of the metazoan infections also seem to be associated with the produc- 
tion of a hemolytic and perhaps other poisons, and the metazoa 
often serve also as hosts carrying pathogenic bacteria into the human 
subject. Many questions concerning the zooparasite infections, how- 
ever, await elucidation, not only those pertaining to etiological factors 
and the modes of transmission, but also those relating to natural and 
acquired immunity. 

Diagnosis. — Many of the infections may be recognized with certainty, 
others with relative certainty, by means of their clinical manifestations — 
which are discussed under the respective headings. In addition, the 
progress of medical science during recent years has rendered available 
several more or less specific diagnostic methods. Many infections 
of known etiology may be diagnosticated without doubt by isolating 
from the patient the specific causative microorganism. This may be 
found on or in more or less superficial lesions of the skin or accessible 
mucous membranes, in the blood, in the cerebrospinal fluid, in fluid 
removed by puncture from the serous sacs, in the organs and tissues 
of the body, in discharges, etc.; and the microorganisms may be studied 
in coverslip preparations or by cultural methods. As already stated, 
the agglutinins are the active factor in causing agglutination of bacteria, 
a phenomenon utilized in the Gruber-Widal reaction — the agglutination 
or clumping of microorganisms when added, in dilutions of 1 to 50 
to 1 to 1000 or more, to blood serum containing specific agglutinins. 
This is an important diagnostic test in typhoid fever, paratyphoid fever, 
relapsing fever, Malta fever, bacillary dysentery, cholera, plague, 
glanders, tuberculosis, etc. The presence of bound or unbound com- 
plement is utilized as a basis of the Wassermann complement-binding 
(or deviation-of-the-complement) test in the diagnosis of syphilis and 
so-called parasyphilitic disorders, like tabes dorsalis and paretic de- 
mentia; its use has been suggested also in typhoid fever, meningo- 
coccic and gonococcic infections, trypanosomiasis, echinococcic disease, 
carcinoma, etc. The reaction, which is based upon original observa- 
tions of Bordet and Gengou, requires for its successful carrying out 
much experience and laboratory facilities. In brief, it consists of adding 
to the blood serum of a patient suspected of being syphilitic a watery 
extract of a syphilitic (usually foetal) liver (or other organ containing 
Treponema pallidum); if the patient is syphilitic, the blood serum 
contains syphilitic antibodies or amboceptors and the complement is 
bound. If this mixture be now added to sheep's erythrocytes and the 
corresponding amboceptors, hemolysis does not occur — the available 
complement (necessary to complete the hemolysis) being already 
bound. Recently it has been found that extracts of normal liver, 
sodium glycocholate, lecithin, and other lipoids may be utilized 
instead of the original antigen (syphilitic liver); and more recently 
Noguchi has modified the test by substituting an antihuman for the 
original antisheep hemolytic system, and by utilizing test papers 



PROPHYLAXIS OF THE INFECTIONS 29 

saturated with antigen, amboceptor, and complement. Finally, it has 
been found that under the influence of bacterial toxins and other antigens, 
certain animals and human subjects develop a specific hypersensitive- 
ness to the antigen in question (anaphylaxis), so that a second injection 
of the antigen may bring about serious and sometimes fatal results, 
although the two doses combined were less than that ordinarily provoca- 
tive of toxic results. Such a phenomenon is sometimes observed in 
human subjects after the injection of diphtheria and other antitoxins, 
the serum and not the antitoxin as such being the active factor (serum 
disease or fatality). In tuberculosis, glanders, and other infections 
the tissues also become sensitized to the toxin in question, so that when 
an extra amount is added they react variously; this is the basis of the 
various tuberculin reactions, the mallein reaction, etc. 

Prophylaxis. — The prevention of the infections is no less important 
than their cure, and since each case presupposes an antecedent case, 
efforts should be made to throttle the disease at its source. This, the 
individual patient, is the practising physician's chief concern. The 
patient should be isolated. So imperative is this in infections, such 
as smallpox, scarlatina, diphtheria, typhus fever, yellow fever, cholera, 
plague, etc., that isolation and supervision is one of the readily conceded 
functions of the health authorities, is ordered by law, and in the best 
regulated communities is effected in special hospitals provided for the 
purpose. It is equally desirable that isolation should be practised in 
other infections, which if they do not create the communal consterna- 
tion that pertain to those already mentioned, still have a greater mor- 
bidity and often a larger death toll — that is, typhoid fever, measles, 
rubella, pertussis, cerebrospinal fever, puerperal fever, pneumonia, 
tuberculosis, gonococcic infection, syphilis, etc. If treated at his home, 
the patient should be placed in a large, clean, quiet room, provided 
with an abundance of sunlight and fresh air, and adequately protected 
against flies, mosquitoes, and other insects; all unnecessary furniture, 
carpets, hangings, pictures, etc., should be removed; and a sheet, wet 
with carbolic acid, mercuric bichloride, or formalin, may be hung before 
the door, if for no better purpose than to warn away the inquisitive. 
In the readily transmissible infections (diphtheria, scarlatina, small- 
pox, etc.) the patient should be provided with at least one, preferably 
two, nurses or attendants; all other persons should be rigidly excluded 
from the sick room. The nurses, as well as the physician, prior to 
entering the sick room, should don a gown that entirely envelops the 
body and should cover the head; and on leaving the room and removing 
the gown, they should wash the exposed parts of the body (hands and 
face). The nurses should also wash their hands after touching or 
handling the patient; or they may protect themselves by wearing rubber 
gloves. Similar precautions should be adopted also in the less readily 
transmitted infections, notably typhoid fever, tuberculosis, etc. 

In all cases of infection, the patient's personal linen, bed-linen, 
dishes, knives, forks, spoons, etc., should under no circumstances 



30 INFECTIOUS DISEASES 

be placed in contact with those used by other members of the house- 
hold; nor should the attendants upon the patient prepare food for 
other members of the family. All dishes and other utensils used 
by the patient (such as the bed-pan, urinal, etc.), should be dis- 
infected after use, by boiling or the use of a 5 per cent, carbolic 
acid solution. All discharges from the patient, such as from the 
mouth, nose, or ear, the urine, feces, sputum, vomitus, etc., should 
be destroyed : if possible, by incineration and complete destruction, or, 
when this is not available, by the use of milk of lime, carbolic acid 
(5 per cent.), or mercuric bichloride (1 to 500 or 1 to 1000). The 
milk of lime must be freshly prepared by adding to a lump of quicklime 
about half its volume of water; the resulting hydrate should be kept 
sealed, and as required one part of it should be added to four to six 
parts of water. Whichever disinfecting solution is used should be 
added to the discharge in the proportion of two to three volumes to one, 
thoroughly mixed, and allowed to act for two to six hours before being 
emptied into the closet. Throughout the course of the infection, the 
patient's personal and bed-linen, etc., should be put directly from the 
bed into a large sheet and then into carbolic acid (5 per cent.), or 
mercuric bichloride (1 to 500); thence it should be removed to a suitable 
place and boiled for at least one hour. 

After the patient has recovered, he may be given a bichloride bath 
(1 to 2000), and his skin may be anointed with olive oil; he should 
then be removed to another room, previously well aired, and fresh linen 
should be provided. Should death occur, the body should be enveloped 
in several sheets or other cloths wet with carbolic acid (5 per cent.) 
or mercuric bichloride (1 to 500), and as soon as possible placed in a 
coffin and hermetically sealed. After convalescence (or death) the 
room and its contents must be thoroughly disinfected. The preferable 
method for the contents is by incineration and complete destruction; 
this is desirable especially for old mattresses, carpets, rugs, hangings, 
and other articles of little value; articles of value may be subjected to 
the action of superheated steam (steam under pressure), or boiling 
water, or chemicals, such as carbolic acid, mercuric bichloride, or 
formaldehyde. The room itself should be hermetically sealed and 
subjected to the action of formaldehyde gas, which may be generated 
in special generators, or by the addition of potassium permanganate 
to the official formalin, in the proportion of 8 ounces (250 grams) of 
the permanganate to one pint (500 c.c.) of the formalin to each 1600 
cubic feet of air space. The room should not be opened until after 
the lapse of twelve to twenty-four hours. Thereupon the floor and 
other woodwork, etc., should be scrubbed with hot water and soap, 
and then washed with mercuric bichloride (1 to 500) — which some 
time after it has dried should itself be washed off. The room then 
should be exposed for a day or two to a vigorous current of fresh air 
and as much sunlight as possible. New wall paper should be sub- 
stituted for the old. 



TREATMENT OF THE INFECTIONS 31 

In addition to the aforementioned measures, which are designed to 
prevent the spread of infection, there are other important prophylactic 
procedures. These comprise, particularly, a pure, non-infected water 
supply, which is especially important as regards typhoid fever, dysen- 
tery, cholera, etc. The water should be taken from a source as pure as 
possible, and in the event of even the slightest doubt, should be filtered 
(chemical disinfection does not seem to be as efficacious as filtration, 
and is otherwise objectionable). During the prevalence of an epidemic 
all the drinking water should be boiled, and only boiled water should 
be used for washing the teeth, as well as foodstuffs, like celery, lettuce, 
etc. Special care must be taken to see that other articles of diet are 
not contaminated; such as milk (diluted with infected water or handled 
in dairies where an infection prevails); oysters and other shellfish 
grown in polluted streams; vegetables grown in infected ditches or 
watered or washed with infected water; meats from diseased animals, 
etc. These if eaten at all must be thoroughly cooked. Attention must 
be paid to the existence of chronic "carriers," who are often responsible 
for local or widespread epidemics of typhoid fever, dysentery, etc., as 
well to the slight sore throat (diphtheria, scarlatina) and the persisting 
nasal and aural discharges that often follow diphtheria, scarlatina, etc. 
In time of war or during peaceful military encampments, additional 
sanitary measures should be undertaken, especially the proper disposal 
of refuse, urine, and feces, the protection of latrines and garbage cans 
from flies and other insects, etc. An efficient prophylaxis of the large 
and increasing number of ill-understood infections in the tropical and 
subtropical regions, some of demonstrated protozoan origin and many 
known to be transmitted by various insects, is to be expected from a 
careful study of the life history of the infection-carrying insects, and 
the adopting of preventive measures in accordance with the discoverable 
facts. Finally, among the prophylactic measures, one must mention 
preventive inoculations, which are resorted to with complete success 
in smallpox (vaccinia), and have been used with encouraging results in 
hydrophobia, typhoid fever, cholera, plague, anthrax in the lower 
animals, etc. 

Treatment. — Since the specific nature of many infections has been 
demonstrated, scientists have labored to produce specific remedies 
that shall, in some measure, at least, reproduce the normal immunizing — 
antitoxic, bacteriolytic, and phagocytic — processes of the body. Some 
are available and of unquestionable utility. Diphtheria antitoxin, the 
first discovered, has virtually revolutionized the treatment of diph- 
theria, and may be looked upon as a specific, certain to cure if resorted 
to early in the course of the infection. The hope born of this success 
has not found fulfilment as regards many of the other infections — 
because antitoxin is efficacious only if resorted to before the toxin has 
formed a firm union with or destroyed the tissues, and because many of 
the bacteria produce not an extracellular toxin, but an intracellular, 
so-called endotoxin, which does not provoke the formation of an anti- 



32 BACTERIAL INFECTIONS 

toxin, although it may lead to the formation of a bacteriolytic sub- 
stance. The tetanus antitoxin, for instance, is usually inefficacious, 
because the development of symptoms is significant of a firm, almost 
indissoluble union between the toxin and the nervous tissues. Success 
has attended the prophylactic use of this tetanus antitoxin in cases, 
such as Fourth-of-July wounds, known to be especially likely to be 
followed by tetanus. The use of pneumococcic, staphylococcic, strep- 
tococcic, and plague antitoxin, as a rule, has not been followed by 
results better than those which attend other forms of treatment, although 
some notable successes have been achieved. Encouraging results have 
followed the use of Flexner's antimeningococcic serum. The use of 
bacteriolytic serums is not to be unreservedly commended, since the 
solution of bacteria in the tissues is not free from danger. Recently 
bacterins (bacterial vaccines ; suspensions in physiological saline solution 
of killed bacteria) have been used with considerable success, especially 
in staphylococcic, streptococcic, pneumococcic, gonococcic, tuberculous, 
dysenteric, some typhoid-colon infections, Malta fever, etc. These bac- 
terins act by facilitating or augmenting an active immunity, and while 
they doubtless favor the production of several immune substances, their 
chief action perhaps is to stimulate the production of specific opsonins, 
and thus to facilitate phagocytosis. Wright believes that the adminis- 
tration of bacterins should be controlled by estimations of the opsonic 
index (the opsonic power of a patient's blood, as compared with that of 
a healthy person, in respect to a given microorganism) ; this in practice, 
however, has not been found necessary. Autogenous vaccines are much 
more efficacious than stock vaccines. Recently also Hiss, acting upon 
the hypothesis that the activity of the phagocytes in the processes of 
immunity is due, in part at least, to the presence of an intracellular 
antitoxin (endo-antitoxin), has suggested the use of aqueous extracts of 
washed dead leukocytes in staphylococcic, streptococcic, pneumococcic, 
meningococcic, and other infections. Encouraging reports of the effi- 
cacy of the treatment have been made. But all methods of specific 
therapy are still on trial; the final pronouncement regarding their 
value is reserved for the future. 



BACTERIAL INFECTIONS. 

TYPHOID FEVER. 

(Enteric Fever; Abdominal Typhus.) 

Typhoid fever is an acute, specific, infectious disease caused by 
Bacillus typhosus (Eberth-GafTky) ; it is a true bacteremia, characterized 
anatomically by hyperplasia and necrosis of the lymphoid tissues of the 
body, especially of the intestinal tract, and clinically, by slow onset, 
continued fever of characteristic type, enlargement of the spleen, a 



TYPHOID FEVER 33 

characteristic roseolous rash, a specific serum reaction, the so-called 
typhoid state, and a tendency to relapse and to the occurrence of 
certain complications, notably intestinal hemorrhage and perforation. 

Etiology. — While typhoid fever occurs at all ages, even in infancy 
and in old age, it is especially frequent between the ages of fifteen and 
thirty years ; but typhoid infection may occur even in utero. It is equally 
common in both sexes, and affects persons in all stations of life. It 
occurs in all parts of the world, but is especially prevalent in the temperate 
and subtropical zones. It is endemic in most large cities and frequently 
prevails epidemically, especially in the autumn and early winter — more 
commonly after a dry, hot summer (whence the term autumnal fever) ; but 
in some localities the disease is quite frequent in the spring, concurrent 
with the thaws and floods. Newcomers in infected localities are espe- 
cially susceptible, more particularly those who move from the country 
to the city. Bad sanitary arrangements, familial and municipal, such 
as defective drainage, contaminated water supply, poor ventilation, 
the accumulation of filth, etc., act as predisposing factors — favoring the 
development of the typhoid bacillus and reducing the vitality of the 
individual. Pettenkofer attributed the development of the disease to 
the condition of the " ground soil," believing that a low level of the 
standing water favors the occurrence of the disease. One attack usually 
confers more or less absolute immunity, but recurrences are by no means 
unknown. Some persons seem to possess a natural immunity. The 
immunity of old residents in infected localities, however, is frequently 
due to their having had the disease in early life — when the symptoms, 
as a rule, are mild and the mortality low. 

The exciting cause of the disease is Bacillus typhosus. Infection 
is almost exclusively transmitted by infected food or infected drink; 
sometimes by direct contact, by a third person, by the air, by fomites, 
or by infected animals. Every case of the disease thus presupposes 
the existence of some previous case, that directly or indirectly act& as 
a source of infection; many widespread and fatal epidemics have been 
traced to a single case. Infection is commonly acquired by way of the 
gastro-intestinal tract; rarely perhaps by way of the respiratory tract. 
In the usual, that is, the gastro-intestinal cases, the infectious atrium 
has not been definitely determined, the ileum, the upper part of the 
intestine, the stomach, and the tonsils being variously looked upon as 
the portal of entry of the bacillus. For obvious and good reasons the 
ileum is generally believed to be the portal of entry, but as opposed to 
the correctness of this view one may perhaps adduce the early bac- 
teremia (as early as the fourth day) when changes in the lymphoid 
follicles of the ileum are slight, and the early disappearance of bacilli 
from the feces: they are believed not to thrive well in the intestinal 
contents and those present not improbably come from the gall-bladder 
and the bile into which they are promptly excreted from the blood. 
Infection by way of the gastro-intestinal tract results from the swallow- 
ing of infected food or drink, especially water, milk, oysters, and the 
3 



34 BACTERIAL INFECTIONS 

like. The drinking water usually becomes contaminated by soakage of 
infected sewage, feces, or urine into wells, cisterns, springs, reservoirs, 
rivers, etc. Milk is usually contaminated by being diluted with infected 
water, or by being put into utensils washed with infected water; or it 
becomes infected from the unclean hands of dairy attendants or other 
persons. Derivatives of milk, such as cream, ice cream, butter, etc., may 
also serve as sources of infection, as well as articles of food that have 
been washed with contaminated water, or that may be eaten raw, such 
as oysters fattened in polluted streams, and lettuce, celery, etc., grown in 
contaminated ditches or watered with contaminated water. Food may 
also become infected by flies and other insects, to whose feet the bacillus 
readily adheres or whose feces may contain the specific germ. This 
occurs especially in rural districts, the family privy vault often being 
the source of infection; in warm climates; and during army movements, 
the flies conveying the bacillus directly from latrines to the kitchen or 
mess table. 

Direct transmission from the sick to the well sometimes occurs (one- 
fourth of the cases Conradi), and is apparently the only cause that can 
be assigned for some cases of the disease occurring in nurses, attend- 
ants, etc. The emanations from the patient are not necessarily infective; 
but the stools, urine, etc., are not properly disinfected, and infect the 
bed-clothing, the patient's personal linen, etc., and these being incau- 
tiously handled, serve as the indirect source of infection. A number of 
cases, even restricted epidemics, have recently been traced to so-called 
"carriers," subjects of past typhoid fever, whose feces may contain the 
typhoid bacillus continuously or intermittently (chronic or intermittent 
carriers). The feces become contaminated from the gall-bladder, which 
may remain a permanent habitat of the bacillus. 

Infection by way of the respiratory tract is relatively uncommon. That 
it is possible cannot be denied (some cases of apparently primary typhoid 
pneumonitis). However, bacilli in the air being inhaled are usually 
arrested in the pharynx and eventually gain the gastro-intestinal tract — 
whence infection occurs, as is usual. It is possible that in rare instances 
infection may occur through the tonsil, and the blood thus become 
primarily infected (certain cases of typhoid fever without intestinal 
lesions?). 

Pathology. — The characteristic macroscopic lesions of typhoid fever 
involve the solitary and agminate lymph follicles of the intestine, the 
mesenteric and other lymph nodes, and the spleen. The typhoid bacilli 
having reached the intestine doubtless invade the lymphoid tissues, the soli- 
tary and agminate follicles, thence the mesenteric lymph nodes, and ulti- 
mately become dispersed through the lymphatic and the blood circulation 
and all the organs of the body. The changes in the lymph follicles of the 
intestine are commonly said to exhibit four stages — infiltration, necrosis, 
ulceration, and cicatrization — which correspond approximately to the 
four weeks of the disease, but approximately only, since the different 
processes may be shortened or markedly prolonged, and in some cases 



TYPHOID FEVER 35 

the lesions may not proceed beyond infiltration, resolution occurring 
soon. At the end of the first week, Peyer's patches are swollen, hyper- 
emic, and the seat of endothelial and lymphoid proliferation. They 
appear as flat, raised patches, of pinkish-gray color, somewhat soft in 
consistency, and with a smooth or rugous surface. During the second 
week more or less complete necrosis of the solitary and agminate follicles 
takes place — yellowish-green and greenish-brown sloughs (stained with 
bile) being formed. During the third week, by a process of ulcera- 
tion, the slough is gradually separated and a more or less characteristic 
ulcer results. These ulcers are ovoid in shape (Peyer's patches), their 
long axis being in the direction of the long axis of the bowel; roundish 
ulcers (solitary follicles) are also quite frequently seen. The edge of the 
ulcer is undermined, its floor is smooth and made up of the muscular 
coat of the intestine or of the peritoneum. In some cases the latter 
is involved in the necrotic process and eventually becomes perforated. 
During the fourth week cicatrization ensues; it may be complete within 
a week or ten days, or it may be unduly protracted and become chronic. 
Often side by side one sees lesions in different stages of progress. Some- 
times the cicatrices are visible for years — as a thinning of the mucous 
membrane, absence of the intestinal villi, and the presence of pigment. 

These lesions while most common in the lymphoid tissues of the 
intestine, especially of the lower part of the ileum, occur throughout the 
body. The incidence of occurrence in different parts of the body is well 
exemplified by the following table, compiled by Baer, which gives in 
percentages the results of an analysis of the sites of ulcerations in over 
1400 typhoid-fever necropsies : Small intestine (any part), 97.5; ileum, 
89; ileum alone, 53.3; ileum (lower half), 36.8; large intestine, 33.3; 
cecum, 30.3; colon (not specific), 29.1; larynx, 19.9; ascending colon, 10.3; 
sigmoid flexure, 6.9; ileocecal valve, 6.7; jejunum, 5.9; large intestine, 
alone, 5.6; transverse colon, 4.5; cesophagus,4.5; descending colon, 2.6; 
vermiform appendix, 2.5; rectum, 2.4; pharynx, 2.2; cases without ulcera- 
tion, but proved bacteriologically, 2.2; stomach, 1.98; Meckel's diver- 
ticulum, 1.1; trachea, 0.38; duodenum, 0.3; common bile duct, 0.23. In 
some cases the intestinal lesions are widespread and extensive; in other 
cases they are so slight as to be scarcely detectable; in some cases they 
are altogether absent — typhoid fever without intestinal lesions (typhoid 
bacteremia or septicemia). 

The mesenteric lymph nodes, especially those corresponding to the 
portion of intestine affected, become hyperemic and swollen, largely 
in consequence of endothelial and lymphoid proliferation. Generally 
resolution takes place, but occasionally they become softened and 
necrotic, and may rupture into the peritoneum, causing peritonitis, 
or they may become caseous, calcareous, or atrophic. The lymph 
nodes throughout the body sometimes are swollen, and the superficial 
nodes may be palpable. The spleen becomes markedly enlarged 
(two or three times its normal size), its capsule tense, the pulp dark, 
reddish brown in color, and almost diffluent, and the Malpighian bodies 



36 BACTERIAL INFECTIONS 

prominent. Usually it returns to its normal condition, but infarction 
and abscess formation may ensue. 

Our knowledge of the nature of the foregoing lesions has been much 
enhanced by the studies of Mallory, who states that the essential lesion 
in typhoid fever is a diffuse proliferation of the endothelial cells giving 
rise to large epitheloid cells characterized by the possession of marked 
phagocytic properties, and that while this proliferation is most marked 
in the lymphoid tissue of the intestine, the mesenteric lymph nodes, 
the spleen, the bone marrow, and the liver, it may be found also to a 
varying extent in all the lymphatic vessels of the body, as, for instance, 
the lymphatics of the heart, lungs, testicles, pia-arachnoid, etc. The 
cause of these proliferative changes is a mild, diffusible toxin (an 
endotoxin, liberated upon disintegration of the typhoid bacilli) 
which circulates in the lymphatic and the blood stream. The swell- 
ing of the lymphoid nodes of the intestine, the mesenteric nodes, 
and the spleen is due almost entirely to these phagocytic cells, and 
the necrosis is purely accidental, resulting from occlusion of the veins 
and capillaries by fibrinous thrombi the consequence of degenera- 
tion of phagocytic cells beneath the lining endothelium of the vessels. 
These phagocytic cells enter the general circulation, passing through 
the liver and the lungs, on the one hand, and through the thoracic duct, 
on the other. Focal collections of these cells are found in different 
organs, the liver, the kidneys, the heart, the testicles, where they obstruct 
either the capillaries, the veins, or the lymphatics. Certain noteworthy 
changes occur in the bone marrow, as has recently been pointed out by 
Longcope: lymphoid proliferation, large phagocytes, foci of necrosis, 
more or less hyperplasia of the blood-forming cells, and, in the fatal cases, 
diffuse degenerative changes of the blood-forming cells, associated with 
marked oedema and congestion. Longcope suggests that these changes 
may be in some way related to, and perhaps responsible for, the leuko- 
penia of typhoid fever. 

In addition to the foregoing essential and characteristic lesions of 
typhoid fever, others often occur — the result of long-continued fever 
and toxemia and of secondary infection with pyococci — such as paren- 
chymatous degeneration of the liver, kidneys, heart, voluntary muscles 
(Zenker's degeneration, especially of the abdominal muscles and the 
adductors of the thigh), etc. A mild grade of interstitial hepatitis some- 
times develops; the so-called lymphomatous or acute interstitial non- 
suppurative nephritis may occur; the gall-bladder may become inflamed, 
ulcerated, and even perforated (usually infection by way of the portal 
circulation); laryngeal ulceration may progress to and cause ulceration 
of the cartilages and perichondritis; hypostatic congestion of the lungs, 
and lobular or lobar pneumonia or pleuritis may supervene ; cystitis and 
pyelitis, due to typhoid bacilluria, may arise; and thrombosis, especially 
of the veins of the lower extremity, said by Mallory to be due to the 
same sort of lesions that cause occlusion of the vessels in the intestine, 
may occur. In addition, abscesses in different parts of the body, peri- 



TYPHOID FEVER 37 

ostitis, peripheral neuritis, meningitis, orchitis, parotitis, etc., have been 
observed. These, though often the consequence of mixed infection with 
pyococci, are sometimes due to the typhoid bacillus alone, and, as for 
instance in periostitis, they may remain dormant for a long time — months 
and years. 

In the living subject the typhoid bacilli may be found in the stools, 
especially from the end of the first to the middle of the third week, during 
some relapses, and sometimes for months or years after an attack of 
typhoid fever (so-called typhoid carriers); in the urine, especially in cases 
of albuminuria, sometimes for long periods, even months, after con- 
valescence; in the gall-bladder, during and for months or years after 
an attack of typhoid fever (the usual habitat of the organisms in the 
chronic typhoid carriers); in the blood from the spleen, the rose spots, 
and the peripheral circulation; sometimes in the sputum; in the cerebro- 
spinal fluid in the event of certain complications, etc. In many of the 
complications and sequels, especially in post-typhoidal abscesses of the 
bones, subcutaneous tissues, etc., the bacilli may also be. found, but 
they are usually associated with different pyococci. After death the 
typhoid bacilli have been found in the intestine, Peyer's patches, mesen- 
teric lymph nodes, spleen, liver, kidneys, meninges, myocardium, bone 
marrow, blood, lymph, and divers complicating lesions. 

Symptoms. — The period of incubation varies, as a rule, between ten 
and fourteen days, but it may be as short as five, or as long as twenty- 
one or more days. Occasionally this period is unannounced by symp- 
toms. Usually, however, there are prodromes, such as malaise that 
increases with the onset of the febrile stage, headache, insomnia, anorexia, 
sometimes diarrhoea, and, especially in children, vomiting. In most 
cases the onset of the disease is insidious, the patient complaining of 
gradually increasing malaise, disinclination to exertion, headache, neuro- 
muscular pains in the back and limbs, anorexia, epistaxis, possibly 
chilly sensations and f everishness ; finally, he takes to bed — from which 
day we date, though often incorrectly, the onset of the disease. Occa- 
sionally the onset is sudden and manifested by severe headache, pains in 
the back and legs, chills that may be repeated, marked prostration, etc. 

During the first week the symptoms mentioned become aggravated; 
the temperature rises in a characteristic step-ladder manner; the tongue, 
though it remains moist, becomes furred; the pulse becomes increased in 
frequency (90 to 100); there is thirst; the abdomen becomes distended and 
tender on pressure; though there may be diarrhoea, constipation is the 
more likely; and there may be slight cough due to bronchitis. 

At the end of the first week, sometimes by the fourth or fifth day, the 
fastigium is reached. All of the symptoms become aggravated; the 
temperature reaches its highest point (usually 103° to 104° F.), and 
it remains high, the daily remissions being less than during the first 
week; the pulse becomes accelerated, 90 to 110, and dicrotic (an early 
feature) ; the headache gives way to mental hebetude and later to delirium, 
especially at night; the patient is often quite deaf; and the typhoid state 



38 BACTERIAL INFECTIONS 

frequently supervenes. The skin is usually hot and dry, but frequent 
attacks of profuse perspiration, followed by sudamina, may occur. 
About the eighth day of the disease a number of rose-colored spots, 
that are quite pathognomonic, appear on the abdomen, the chest, and 
frequently elsewhere, especially on the back. The spleen is enlarged, dis- 
tinctly palpable, and somewhat tender. The tongue becomes dry and 
later fissured, and sordes may form on the teeth and gums. The abdo- 
men may become markedly distended, gurgling in the right iliac fossa 
may develop, and the constipation may give way to diarrhoea. The 
stools are of a pale yellow (pea-soup) color and highly malodorous 
(characteristic typhoid stool). The fastigium usually lasts from ten 
days to two weeks. 

Toward the end of the fastigium, that is, in the third week, the typhoid 
state becomes more pronounced, and the pulse more rapid, 110 to 130 
or more; the temperature, previously continuous, becomes remittent, 
and usually somewhat lower than during the second week; and any of 
the many complications may arise. In favorable cases at about the 
twenty-first day of the disease (the commencement of the fourth week) 
the stage of decline or defervescence sets in. The fever lessens and 
finally becomes intermittent with less and less diurnal variations; the 
local and general symptoms abate; and convalescence ensues. 

From the foregoing, which represents in outline the course of an 
ordinary or average case of typhoid fever, there are many departures ; the 
symptoms vary much with the virulence of the infecting microorganisms, 
the resistance of the individual, and the presence or absence of compli- 
cations and secondary infections — due usually to pyogenic cocci. 

The Fever. — In the majority of cases, during the first four or five 
days of the disease, a daily increase of temperature of 1.5° to 2° F., 
and a morning remission of from 1° to 1.5° F., occur — producing what 
is spoken of as the step-ladder or zig-zag course of the fever (Fig. 1). 
The temperature usually reaches its maximum on the fourth, fifth, or 
sixth day. Then follows the fastigium, which lasts usually from ten to 
fourteen days, and during which the temperature is more uniform and 
of the continuous type, the morning temperature being 102° to 103° F., 
and the evening from 103° to 104° F., or higher. In ordinary cases 
toward the end of the fastigium (thirteenth to sixteenth day) the tem- 
perature becomes remittent, and the evening rise shows some tendency 
to be less marked. At the end of the fastigium (sixteenth to twenty- 
first day) the temperature is usually intermittent ; the morning temperature 
approaching if not quite reaching the normal, and the evening tem- 
perature being 101° to 101.5° or 102° F. Gradually the evening 
temperature also becomes normal. In cases of moderate severity 
the temperature may begin to decline at the end of the second week 
and soon reach normal; in severe cases it may remain high (104° to 
105° F.) in the evening throughout the third week, even into the fourth 
week, and then gradually decline. Defervescence occurs usually by 
lysis, rarely by slow crisis. 



TYPHOID FEVER 



39 



Variations in the course of the temperature, however, are quite 
common. Thus, the early step-ladder rise may be missed. During 
the greater part of the fastigium the temperature may be 105° to 
106° F. or more (hyperpyrexia). Even higher temperatures are 
occasionally met with — 107°, 109°, 110° F., especially in the event 
of certain complications, such as pneumonia, septic manifestations, 
pyococcic infections, etc. Again, the fever may be unduly protracted, 
continuing four, five, six, or more weeks — usually the consequence of 
certain inflammatory complications (secondary infections), such as 
suppurating mesenteric lymph nodes, or sluggish intestinal ulcers, post- 
typhoidal anemia, intestinal auto-intoxication, etc. Sometimes the 

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The temperature curve and the chief symptoms in typhoid fever. (Musser.) 

temperature is distinctly intermittent throughout the course of the 
disease, even in the absence of complicating malaria. In other cases the 
fever may be slight throughout the entire course, or the temperature may 
be scarcely above normal (apyrexial form), or even subnormal. It is 
quite often subnormal during convalescence. 

Sudden temporary falls of temperature are sometimes met. They 
are due to: (1) Intestinal hemorrhage; (2) intestinal perforation; (3) 
cardiac failure or vasomotor collapse; (4) abortion or premature labor; 
(5) the use of coal-tar products; (6) ill-understood nervous factors; and 
(7) they sometimes occur without obvious cause. 

Post-typhoidal elevations of temperature (recrudescences) are quite 
common. They sometimes occur during the period of defervescence, 



40 BACTERIAL INFECTIONS 

but more frequently during convalescence — after the morning and 
evening temperatures have been normal for several days. The recrudes- 
cence often occurs rather suddenly, the temperature may reach a 
high grade (103° to 105° F.), but usually it subsides within three or four 
days, although it may last a week. Such recrudescences are attrib- 
utable to dietetic errors, constipation (auto-intoxication), emotion and 
excitement attending the visits of too solicitous friends, etc. If pro- 
tracted the fever is significant of some complication, or of anemia, or 
it may be what has been aptly termed "bed fever" — due to low diet 
and too prolonged stay in bed. 

Chills, according to Osier, occur (a) sometimes with the fever of onset ; 
(b) occasionally at intervals throughout the course of the disease, and 
followed by sweats (so-called sudoral form); (c) with the advent of 
complications, pleurisy, pneumonia, otitis media, periostitis, etc.; (d) 
with active antipyretic treatment by the coal-tar products; (e) occasion- 
ally during the period of defervescence without relation to any complica- 
tion or sequel, probably due to septic infection; (/) according to Herring- 
ham, chills may result from constipation ; there are some cases in which 
during the latter half of the disease chills recur with great severity. 

Skin. — In from 75 to 85 per cent, of all cases a characteristic roseolous 
rash appears on the body on from the seventh to the ninth day; rarely 
it may be delayed to the twelfth day. It consists of isolated, circular, 
slightly elevated macules or maculo-papules, from 2 to 4 mm. in diameter. 
They are found almost always on the trunk, especially on the abdomen 
and the lower chest; but their absence should not be certified to until the 
back has been thoroughly examined. Sometimes they are present on 
the arms and the legs, and the face; occasionally in large numbers. They 
disappear upon pressure and reappear immediately the pressure is 
removed. Usually they come out in successive crops, each crop con- 
sisting, as a rule, of from six to a dozen or more spots. Each spot lasts 
about four or five days, so that fading spots are seen side by side with 
others of a newer crop. They continue to appear until the end of the 
second week; sometimes even in the third week, and occasionally during 
convalescence; and they are, not infrequently observed during a true 
relapse. In some cases they are entirely absent; in other cases they 
are numerous and cover the entire body. When numerous they are 
usually darker than when fewer; occasionally they are hemorrhagic. 
A fine, furfuraceous desquamation is not infrequent; occasionally the 
desquamation is flaky. 

Other eruptions are often encountered. Thus sudamina and miliaria 
are common, especially during the second and the third weeks; they 
are usually associated with profuse perspiration and not infrequently 
with chills — sudoral typhoid, of the French. A diffuse scarlatiniform 
erythematous rash (in some cases undoubtedly a drug eruption) has 
sometimes been observed, especially during the first week. Morbilliform 
rashes, urticaria, and herpes are occasionally seen. Rarely one en- 
counters, especially on the abdomen, small bluish spots that do not 



TYPHOID FEVER 41 

disappear on pressure (maculae cerulese, laches bleudtres of Trousseau, 
or peliomas) ; they have been attributed to, but are probably not always 
due to, pediculi. Again, petechia? and purpuric spots occur, especially 
in debilitated subjects; and rarely even extensive gangrenous dermatitis 
(due, doubtless, to infection of the skin), of which I have seen a 
number of cases. More or less extensive furunculosis is not uncommon. 
Bed sores are not so common as formerly — due to improved nursing; 
but they may occur in debilitated subjects, especially if the disease be 
protracted. Loss of the hair and cessation of the growth of the nails are 
not uncommon. (Edema of the skin and subcutaneous tissues may 
result from venous thrombosis, anemia, or nephritis. 

Digestive System. — The tongue is usually coated throughout the 
course of the disease ; at first moist, it soon becomes dry, swollen, brown, 
and fissured. I have seen severe acute glossitis. The gums are not 
infrequently covered with sordes (epithelial debris, food particles, 
bacteria, etc.). Stomatitis progressing to hemorrhage and ulceration 
may ensue. Parotitis, unilateral or bilateral, and due to extension of 
infection along Stenson's duct or rarely to metastatic pyogenic infection, 
is occasionally observed. Extension of infection along the Eustachian 
tube may result in suppurative median otitis. Cancrum oris is rare; 
I have seen a case from which the diphtheria bacillus was isolated. 
Sore throat is sometimes complained of; the tonsils may be swollen 
and congested, and present whitish spots of lacunar or other inflamma- 
tion which may proceed to ulceration (tonsillar typhoid). Catarrhal 
and ulcerative pharyngitis and oesophagitis are by no means infrequent, 
and may be followed by stenosis. Anorexia is the rule. Nausea and 
vomiting are unusual, although they may be present at the outset, and 
have been known to recur about the third week or to continue throughout 
the course of the disease, and to contribute to the fatal issue. The 
gastric juice is deficient in amount, and hydrochloric acid is usually 
much diminished or absent. While diarrhoea may be present at the 
beginning and continue throughout the course of the disease, constipa- 
tion is the rule at the onset and not infrequently persists. Usually, 
however, at about the end of the second week, if not earlier, diarrhoea 
(four to ten or more stools in the twenty-four hours) appears; but even 
marked constipation may be present with even extensive ulceration of the 
ileum. The diarrhceic stools are quite characteristic: of the color and 
consistency of pea-soup, alkaline, and very malodorous; usually they 
separate on standing into an upper turbid liquid layer, and a lower thick 
sedimentary layer, consisting of partly digested food, desquamated, 
epithelial cells, necrotic-tissue elements, blood corpuscles, granular debris, 
triple phosphate crystals, and numerous bacteria. Cultures may reveal 
the typhoid bacillus. 

Tympanites is common, but rarely nowadays so marked as to be 
grave. When marked, by interfering with the action of the diaphragm, 
it occasions dyspnoea, and may embarrass the heart, and also favor 
intestinal perforation. Gurgling and pain on pressure may be found 



42 BACTERIAL INFECTIONS 

in the right iliac fossa. Spontaneous pain in the abdomen is present in 
about one-third of the patients, and contrary to former opinions accord- 
ing to which it was believed always to indicate or suggest perforation 
and peritonitis, it may be due to a wide variety of diseased conditions : 
it is not infrequently due to extra-abdominal conditions, such as pleurisy 
or pneumonia, or even femoral phlebitis ; it is a not infrequent concomi- 
tant of an enlarged spleen, of a distended urinary bladder, of severe 
diarrhoea or marked constipation, and sometimes it attends intestinal 
hemorrhage. Usually, however, it suggests serious complications, of 
which the most important are intestinal perforation, appendicitis, and 
cholecystitis. 

Intestinal hemorrhage occurs in from 3 to 7 per cent, of the cases. 
It is rarer in children. It may occur at the end of the first week, when it 
is usually slight and due to marked congestion; usually it occurs toward 
the end of the second week, or during the third week, or later. The 
hemorrhage may occur once or repeatedly; and the amount of blood 
lost may be so slight as almost if not quite to elude detection, or so extreme 
as to lead immediately to a fatal termination (a rather unusual event). 
Slight hemorrhages are unattended by subjective symptoms; large 
hemorrhages are indicated by sudden and rapid fall of the temperature 
(2° to 8° F.), pallor, a sensation of faintness, a rapid and small pulse, 
low and falling blood pressure, extreme prostration, and visible blood 
in the stools (though even death may occur without the discharge of 
blood from the bowel). Clinically, a single, even rather large, hemor- 
rhage is not necessarily a serious phenomenon, since patients often 
improve after a hemorrhage, especially when it occurs early; but 
repeated hemorrhages are likely to lead to a fatal termination. 

Perforation occurs in from 3 to 4 per cent, of the cases, and is re- 
sponsible for one-fourth or more of the deaths. It bears no direct 
relationship to the severity of the infection, since it is not infrequent in 
mild cases, although most common in the severer infections, especially 
those attended by tympanites and hemorrhage. It is more common in 
males than in females, and is rare in children. Although it may occur 
at any time during the course of the disease, even during the first week 
as well as very late during protracted convalescence or relapses, at least 
one-half of the cases occur during the second and the third weeks (most 
commonly in the third week). The perforation involves the ileum in 
88 per cent, of the cases, the colon in 4.7 per cent., and the vermiform 
appendix in 4.7 per cent. (Scott). 

The symptoms of the perforation are those of the rupture (which rarely 
occurs almost if not quite unannounced) and those of the consecutive 
peritonitis (which I have several times seen at necropsy without note- 
worthy clinical signs). The most important symptom of the perfora- 
tion is pain (scarcely missed unless the patient is comatose), which 
usually comes on suddenly, is sharp and paroxysmal in character, com- 
monly situated in the right lower abdominal quadrant, and not infre- 
quently increases in severity for some time. Concurrent with the pain 



TYPHOID FEVER 43 

there are often the usual evidences of collapse (fall of the temperature 
often to or below the normal, increased frequency and smallness of the 
pulse, vomiting, pallor, perspiration, etc.), and subsequently the ordinary 
manifestations of peritonitis. These comprise local pain, tenderness, and 
rigidity of the abdominal muscles, and, as a rule, increasing abdominal 
distention and limitation of the respiratory movements. Replacement of 
the liver flatness by tympany is of value only when it develops rapidly 
and is present in a flat or slightly distended abdomen, and when by 
changing the posture of the patient flatness and tympany alternate; 
even marked tympany may be due merely to intestinal distention. 
Peritoneal exudate may occasion dulness in the flanks, which may shift 
its position with change in the posture of the patient, and may even be 
recognizable by rectal examination. Auscultation may reveal peri- 
toneal frictions, sometimes within a few hours; later there may be an 
entire absence of peristaltic sounds and movements. The general 
signs of peritonitis are often relatively inconspicuous as contrasted with 
the local signs. As a rule, however, the Hippocratic facies, pallid, dusky, 
pinched, and clammy, is present; the temperature soon rises (after the 
initial fall) and becomes intermittent; the pulse-rate and the respiration- 
rate become increased; and hiccough and vomiting sometimes develop. 
Leukocytosis is a valuable, though inconstant, sign. 

Peritonitis may be due also to infection passing through an ulcer 
that has not perforated; to gangrene of the intestine; to softening and 
rupture of a mesenteric or retroperitoneal lymph node; to splenic 
infarction and abscess; to a twisted and necrotic Meckel's diverticulum; 
to cholecystitis, appendicitis, salpingitis, etc. The swollen mesenteric 
lymph nodes are sometimes palpable through the abdominal wall. 

The liver is often enlarged from cloudy swelling, and is occasionally 
somewhat tender. Jaundice is occasionally observed; it may be a toxic 
process or due to cholangitis and obstruction. Cholecystitis is quite 
common, and may occur during the course of the disease or during 
convalescence — when the local signs being in abeyance the condition is 
not infrequently thought to be a " relapse." The symptoms, as a rule, 
however, consist of local pain, tenderness, and muscular rigidity, and 
a palpably enlarged gall-bladder; vomiting sometimes occurs at the 
onset; jaundice is inconstant. Perforation of the gall-bladder is re- 
vealed by pain, fall of temperature, collapse, and consecutive peritonitis. 
Typhoid bacilli are often found in the gall-bladder after death in the 
absence of local disease, and it is to such latent biliary infection that 
many of the cases of true relapse are attributable. Cholelithiasis not 
infrequently follows typhoid fever, and from the gallstones the typhoid 
bacilli have been cultivated. I have observed several cases of primary 
typhoid cholecystitis (recovery of the typhoid bacillus) without other 
evidences of typhoid infection. Suppurative cholangitis, suppurative 
pylephlebitis, and liver abscess have occasionally been observed. 

Respiratory System. — Epistaxis is a significant symptom of the early 
stages of typhoid fever, and occurs usually at the end of the first and the 



44 BACTERIAL INFECTIONS 

beginning of the second week. A simple laryngitis is not very uncommon. 
(Edema, ulceration, perichondritis, and paralysis of the larynx are 
quite rare. Bronchitis is a part of the disease, and one of the early 
manifestations. It is usually slight or moderate in degree only, and 
revealed by cough, slight expectoration, harsh vesicular breath sounds, 
and a few sibilant and fine bubbling rales. Rarely the finer tubes are 
involved — whence bronchopneumonia may supervene. Bronchopneu- 
monia may also follow oedema and congestion of the lungs, which are by 
no means uncommon during the second and third weeks ; during the same 
periods, when the patient is more or less stuporous, an aspiration pneu- 
monia is not infrequent. True croupous pneumonia may also occur during 
the later half of the disease, and is a serious complication. Occasion- 
ally it is an initial manifestation — pneumotyphoid (pneumonia due to the 
typhoid bacillus, with typhoid bacilli in the sputum); in this event the 
early signs are those of pneumonia, the intestinal and other manifesta- 
tions of typhoid fever only developing later. Pulmonary abscess or 
gangrene and pneumothorax are rare sequels. Pleurisy may be primary 
or secondary: secondary to any of the aforementioned pulmonary 
conditions ; primary and due to direct infection with the typhoid bacillus 
— pleurotyphoid. Occurring early, the lesions are usually dry or serous, 
later often purulent. The bronchial lymph nodes have been known to 
soften and suppurate. 

Circulatory System. — The pulse is usually increased in frequency, 
though not proportionately to the fever. During the first week it is 
less than 100, as a rule; in the second week it commonly fluctuates 
below 110 and becomes dicrotic (an early and quite characteristic feature). 
With the progress of the disease the evidences of vasomotor paresis 
become manifest — low blood pressure, increased frequency of the pulse 
(130 or more sometimes), which often becomes running or thready, 
capillary stasis (coldness and lividity of the extremities), overfilling of 
the splanchnic vessels, anemia of the cerebral vessels, and sometimes 
vasomotor collapse. As convalescence sets in vasomotor tone is restored, 
and the pulse becomes slower, fuller, and stronger; during convalescence 
the pulse is often unusually slow (a characteristic feature). Changes 
in the heart muscle (parenchymatous degeneration, and acute interstitial 
myocarditis) are common. Often the only noteworthy clinical manifesta- 
tion is feebleness of the first sound of the heart. When more marked, 
however, there is not infrequently gallop rhythm, or embryocardia, 
or dilatation of the heart (systolic murmur, increase of the dulness, etc.). 
Endocarditis and pericarditis are uncommon, but not unknown. 

Venous thrombosis, especially of the lower extremity (femoral, pop- 
liteal, saphenous, or superficial veins), is not infrequent, particularly 
during convalescence. It may be due to thrombophlebitis (in which 
event the typhoid bacillus may be cultivated from the vein and the 
clot), or to cardiac weakness and slowing of the circulation; the 
more common occurrence of the thrombosis in the left leg may be 
due to the pressure exerted by the right iliac artery crossing the left 



TYPHOID FEVER 45 

iliac vein, as well as to congenital adhesions, which are ten times as 
common in the left as in the right iliac vein. The thrombosis is 
evidenced by swelling and oedema of the leg, and by pain and tender- 
ness along the course of the involved vein. The process usually subsides 
without ill effects, but it may require a long time, and embolism of the 
pulmonary artery, ensuing on dislodgement of the thrombus, has been 
known to result in death. Infarcts of the internal organs are not very 
uncommon, and may result from arterial thrombosis or embolism. 
Gangrene sometimes results from occlusion of one of the larger arteries, 
and a number of cases of more or less local (though sometimes wide- 
spread) gangrene unrelated to definite vascular distribution have 
been reported; they are probably due to secondary infection of the skin 
(gangrenous dermatitis). Heart clot is rather unusual. 

Blood and Hemopoietic System. — Leukopenia is present through- 
out the disease, except in the event of complications, although a temporary 
increase in the leukocytes in the peripheral circulation is not infrequently 
produced by the cold baths. With the leukopenia there is a dispro- 
portionate increase of the large mononuclear leukocytes and a reduction 
of the polynuclear neutrophiles (to 60 per cent, or less). An increase 
of the polynuclear neutrophiles is often an early manifestation of in- 
flammatory complications (perforation, cholecystitis, etc.) and may 
be present with little or no increase in the total number of leukocytes. 
The blood serum agglutinates the typhoid bacillus (Gruber-Widal 
reaction). During the later half of the disease a rather well-marked 
anemia usually develops ; during convalescence this may assume a high 
grade and constitute a serious feature (post-typhoidal anemia). The 
spleen is enlarged and palpable in at least three-fourths of the 
cases. It may extend two, three, or more finger breadths beyond the 
free margin of the ribs, and it is not infrequently quite tender. The 
enlargement is sometimes missed in elderly subjects and in the event of 
perisplenitis. I have seen infarction and abscess of the spleen; rupture 
has been reported. The superficial lymph nodes throughout the body 
are sometimes palpably enlarged. 

Nervous System. — Persistent headache (usually temporal and 
occipital) is a prominent and significant symptom of the first week, and 
is often associated with severe pains and aching in the back and legs. 
During this period also restlessness and insomnia are likely to be present, 
and are often distressing. Sometimes the patient is quite deaf. The 
pupils are usually markedly dilated. Gradually, in most cases, as the 
patient succumbs to the toxemia, that is, during the second week, the 
headache, restlessness, and insomnia are replaced by mental dulness, 
hebetude, and delirium, which vary considerably in different cases, and 
in the beginning at least are usually most marked at night. The patient 
becomes listless and apathetic, and is more or less unconscious of his 
surroundings, although he may lie for hours at a time with his eyes wide 
open (coma vigil); he frequently mutters constantly, picks at the bed- 
clothing or at imaginary objects (carphologia), and exhibits general 



46 BACTERIAL INFECTIONS 

muscular twitchings, especially of the tongue, lips, hands, and fingers 
(subsultus tendinum). Often the undue muscular irritability is quite 
manifest by the ready production of myoidema. In this, the typhoid 
state, the urine and feces may be voided involuntarily, and the patient 
knows not even his wants. Not infrequently he shows a disposition to 
get out of bed — whence he should not be left alone for even an instant, 
as not a few patients have thrown themselves from a window during the 
temporary, though only momentary, absence of the nurse. Occasion- 
ally, instead of a quiet, muttering delirium, the patient may exhibit a 
noisy, hysterical (emotional), or maniacal delirium (especially alcoholic 
subjects, in whom the condition quite resembles delirium tremens). 

Occasionally typhoid fever is ushered in with unusual nervous symp- 
toms. The headache and backache may be intense, and there may be 
also photophobia, pain, tenderness, and rigidity of the muscles of the 
neck, sometimes even retraction of the head, and rarely convulsions 
(more common in children than in adults). In other cases, later in the 
course of the disease, similar symptoms arise. These cases suggest and 
are only with difficulty distinguished from meningitis; three types may 
be distinguished: (1) Cases suggesting meningitis, but in which no 
anatomical lesions can be demonstrated — the so-called meningism of 
the French, probably due solely to toxemia ; (2) cases exhibiting the 
lesions of serous meningitis and perhaps revealing the typhoid bacillus in 
the cerebrospinal fluid ; and (3) cases of purulent meningitis from which 
the typhoid bacillus, either alone or in association with other bacteria, 
may be isolated. Circumscribed encephalitis, and hemorrhage, embolism, 
and thrombosis of the brain (hemiplegia with or without aphasia) have 
been observed. Myelitis or poliomyelitis (spastic or flaccid paralysis) is 
still more uncommon. Peripheral neuritis is quite frequently observed, 
of which a well-known manifestation is the rather common tender 
toes and tender feet — believed to be more common since the use of the 
cold-bath treatment. The very common painful calves (observed fre- 
quently during convalescence), as well as the much less common painful 
muscles in other parts of the body, are not infrequently due to neuritis ; but 
they are sometimes due to myositis or to thrombosis of a vein. Post- 
typhoidal insanity (confusional insanity, melancholia, or mere mental 
dulness) is not uncommon. It is usually attributed to toxemia and 
impaired nutrition, and in the majority of cases soon subsides. Oculo- 
motor paralysis, paralysis of accommodation, iritis, keratitis, conjuncti- 
vitis, and divers other ocular complications have been reported. 

Genitourinary System. — The urine, as a rule, presents the features 
of so-called febrile urine (diminished in amount, high colored, of high 
specific gravity, abundance of urates, etc.). The diazo reaction is usually 
present. At least three-fourths of the patients exhibit slight albumin- 
uria — attributable to toxic degeneration of the renal epithelium. Occa- 
sionally a true nephritis (hemorrhagic or non-hemorrhagic) occurs 
at the height of the disease. I have observed acute interstitial non- 
suppurative nephritis (the so-called lymphomatous nephritis of Wagner). 



TYPHOID FEVER 47 

Nephritis during convalescence or as a sequel is quite rare, the lesions 
developing during the course of the disease usually subsiding in the 
non-fatal cases. Retention of urine is quite common and often occasions 
rather severe abdominal pain. Typhoid bacilluria is present in at least 
one-third of the cases, and sometimes lasts for months after apparent 
recovery from the disease; because the urine is often not disinfected this 
bacilluria is answerable for some epidemics. The bacilluria may be 
due to pyelitis, cystitis, spermatocystitis, prostatitis, or orchitis, or it 
may occur without noteworthy lesions. Diabetes (or glycosuria), hema- 
turia, and hemoglobinuria are rarely observed. Menstruation is not infre- 
quent at the beginning of the disease, and pregnant women usually abort. 

Other unusual complications comprise osteomyelitis, periostitis, peri- 
chondritis, synovitis, and arthritis (from which the typhoid bacillus may 
be cultivated months and even years after the primary infection). Occa- 
sionally during or after convalescence the patient complains of pain, 
tenderness, and rigidity in the lumbar and sacral regions, and of certain 
nervous (sometimes hysterical) phenomena. This condition (so-called 
typhoid spine) is in some cases a pure neurosis, but it not infrequently 
has an organic basis — spondylitis or perispondylitis. Perinephritic 
abscess may simulate the condition. Fever may be an important sign 
in the differential diagnosis. 

Typhoid fever is not uncommonly associated with other diseases, 
especially tuberculosis, malaria, measles, diphtheria, noma, erysipelas, 
furunculosis, etc. Most of the cases of so-called typho-malarial fever 
are true typhoid fever; others are remittent malarial fever; in a few 
cases only do two diseases co-exist. 

Varieties of Typhoid Fever. — Many different varieties of typhoid fever 
have been described; but the infection is always with the same typhoid 
bacillus (which, however, often exhibits variations in certain of its biologi- 
cal characteristics) ; the clinical differences are dependent, therefore, upon 
differences in the virulence of the infecting agent, upon unusual localiza- 
tions of the infection, and upon variations in the resistance of the indi- 
vidual. Thus, mild (typhus lsevis sive lsevissimus, Griesinger) and severe 
forms are readily distinguished. In the mild forms, which are frequently 
overlooked and especially common in children, the clinical and anatomical 
manifestations of the disease are ill developed, and although fever, 
an enlarged spleen, rose-spots, the Gruber-Widal reaction, etc., often 
occur, convalescence is not infrequently established at or before the end 
of the second week; but the disease may run the more usual course of 
three to four weeks. In children the abdominal symptoms are often 
slight or absent, whereas the nervous, cerebral symptoms are likely to be 
marked. 

Unusually acute and rapid cases are sometimes observed. Doubtless 
an abortive form occurs, but it is very uncommon — more especially 
since the general use of the Gruber-Widal reaction. As described, the 
onset presents nothing unusual, except in some cases rather sudden and 
marked initial fever; but at the end of the first week the fever falls, and 



48 BACTERIAL INFECTIONS 

convalescence goes on as in the ordinary cases, though relapses may 
occur. Latent or ambulatory typhoid fever is a form of infection in 
which the symptoms, at the beginning at least, are so mild that the patient 
does not feel the necessity of going to bed, and therefore continues about 
until some unusual phenomenon, such as marked diarrhoea, delirium, 
intestinal perforation, or hemorrhage, etc., brings him under the atten- 
tion of the physician. The subsequent course of the disease is often 
severe and not infrequently fatal. The initial symptoms of typhoid 
fever sometimes suggest an ordinary "cold," influenza, tonsillitis, or 
gastritis. An afebrile, exceedingly rare, form of the infection has been 
described by Liebermeister. The severe cases are characterized, as a 
rule, by unusual severity of the fever and of the nervous symptoms 
(delirium, prostration, vasomotor paralysis, etc.)— whence these are 
sometimes spoken of as the cerebrospinal form. In other cases there 
is unusual localization of the lesions in different organs — whence the 
terms pneumo-typhoid, pleuro-typhoid, nephro-typhoid, tonsillo-typhoid, 
pharyngo- typhoid, meningo-typhoid, etc. A few severe cases have 
been characterized by petechial spots and hemorrhages from the mucous 
membranes — so-called hemorrhagic form. The disease often runs a 
severe course in elderly, alcoholic, and obese subjects. 

Relapses. — A relapse, a repetition of the anatomical and clinical 
features of the diease and due to re-infection, is not an uncommon 
event, occurring in different epidemics in from 3 to 15 per cent, of 
the cases. It should be distinguished from recrudescence of the fever 
(spurious relapse, previously alluded to), as well as from complications, 
such as cholecystitis, pleuritis, etc., for which it is frequently mistaken. 
It is not always possible to discover the source of re-infection: some- 
times it may be from without; usually it is from within, and one 
should always bear in mind the possibility of infection from the gall- 
bladder which frequently harbors typhoid bacilli without obvious local 
disease; the urinary tract also may be the source of reinfection; 
but the real cause of the relapse is most likely to be found amongst the 
problems of immunity — perhaps in temporary exhaustion or over- 
powering of the bacteriolytic activities of the blood. As a rule, the 
relapse comes on within seven days of the beginning of the convalescence; 
sometimes it develops earlier, even before the temperature has reached 
normal (intercurrent relapse), in which event it is often severe and 
protracted; occasionally it may not come on until the temperature 
has been normal for three weeks or more. The period of apyrexia is 
usually without noteworthy manifestations. The onset of the relapse, 
as a rule, is sudden, the temperature rising abruptly, sometimes with 
a chill or chilliness. Then follow usually the characteristic step-ladder 
rise of the temperature (for two or three days), new roseolous spots (on 
the second to the fourth day), and enlargement of the spleen — two of 
which signs, at least, should be present to warrant the diagnosis of a true 
relapse. As a rule, the relapse does not last more than ten or fourteen 
days, and the clinical signs are less severe than in the primary attack; 



TYPHOID FEVER 49 

but occasionally all the phenomena of the disease are much aggravated 
during the relapse, and the patient may die of the toxemia or of one of 
the common accidents, such as hemorrhage or perforation. There may 
be a second, a third, a fourth, and even a fifth relapse. A recurrence, as 
contrasted with a relapse, means another attack of the disease occurring 
after complete restoration to health. Usually, typhoid fever confers 
lasting immunity, but second and apparently well-authenticated third 
attacks have been observed — a period of years intervening between the 
attacks. 

Diagnosis. — The recognition of typhoid fever is, in the one case, a 
matter of the greatest ease, and in another, of the greatest uncertainty 
— for a time at least. No one symptom is conclusive. Of special value 
in the diagnosis are prodromal symptoms lasting for a week or more, the 
gradual onset of fever (of characteristic rise, if it has been observed), 
persistent headache, nose-bleed, roseolous spots, enlarged spleen, early 
dicrotism of the pulse, leukopenia, and the diazo reaction; the diagnosis 
is made conclusive by the Gruber-Widal reaction (in dilutions of 1 to 
50 or more), and the cultivation of typhoid bacilli from the blood, the 
rose-spots, the stools, the urine, or the cerebrospinal fluid. In some 
regions continued fever for seven days without evidence of local disease 
is quite suggestive. Paratyphoid fever, as a rule, is first suggested by the 
absence of the Gruber-Widal reaction with the typhoid bacilli. It may 
be difficult or impossible for some days to exclude cerebrospinal menin- 
gitis, since typhoid fever sometimes begins with severe nervous mani- 
festations, but the characteristic course of the fever, the erythematous 
rose rash (as contrasted with a petechial eruption), the presence of ab- 
dominal symptoms, the absence of herpes facialis, the presence of the 
Gruber-Widal reaction, and the negative results of lumbar puncture, 
serve ultimately to distinguish typhoid fever. The continued types of 
malarial fever, which much resemble typhoid fever, may be distinguished 
by the absence of the Gruber-Widal reaction, the presence of the malarial 
parasite in the blood, and by the administration of quinine. Acute 
miliary tuberculosis is often differentiated with difficulty, but it is sug- 
gested by absence of the characteristic fever curve, of abdominal symp- 
toms, of erythematous rose-spots, of leukopenia, and of the Gruber-Widal 
reaction, and by the presence of increased pulse-rate, of dyspnoea, of 
cyanosis, of ~ occasionally bloody expectoration, of choroidal tubercles, 
and of tubercle bacilli in the cerebrospinal fluid and rarely in the blood. 
Certain pyemic processes, of which ulcerative endocarditis is an example, 
are usually diagnosticated typhoid fever, but they may sometimes be 
differentiated by detecting a source of infection, and by the presence of 
undue dyspnoea, irregular heart action, a peculiar rough systolic, but 
more especially a diastolic murmur, irregular and repeated chills or 
chilly sensations, profuse sweats, the early occurrence of marked prostra- 
tion, the rapid development of anemia, leukocytosis, embolic phenomena 
(petechial hemorrhages, infarctions, etc.), and pyococci in the blood, and 
by the absence of a characteristic fever curve, of persistent headache, 
4 



50 BACTERIAL INFECTIONS 

of epistaxis, of abdominal symptoms, and of the Gruber-Widal reaction. 
Acute leukemia without noteworthy enlargement of the lymph nodes, 
which usually resembles typhoid fever, may be distinguished by the 
absence of the Gruber-Widal reaction and the presence of leukocytosis 
(lymphocytosis). Pneumonia, appendicitis, and tuberculous peritonitis 
also must be considered in the differential diagnosis in certain instances. 

Prognosis. — The prognosis is always doubtful, since no one can fore- 
tell whether or not one of the two accidents (hemorrhage and perforation), 
responsible for almost two-thirds of the deaths, will occur. The mortality 
varies much in different epidemics — from 5 to 12 per cent, in private 
practice to from 7 to 20 per cent, in hospital practice, where the worst 
cases are encountered. During recent years, in consequence of the 
general use of the cold-bath treatment, the mortality has certainly been 
reduced — in some hospital statistics to less than 4 per cent. The prog- 
nosis in general depends upon the severity of the infection, the resistance 
of the individual, and the presence or absence of complications. Aside 
from repeated hemorrhages and perforation (with consecutive peritonitis) 
answerable for almost two-thirds of the deaths, especially unfavorable 
symptoms are persistent high fever, persistently rapid pulse (above 120), 
profound toxemia and delirium, marked tympanites, and complications, 
such as pneumonia, meningism, meningitis, etc. Sudden death may 
occur during the fastigium, as well as during defervescence or con- 
valescence, from cardiac collapse, vasomotor paralysis, pulmonary or 
cerebral embolism or thrombosis, etc. The passage of eighty to one 
hundred or more ounces of urine daily is one of the most favorable 
prognostic signs The prognosis of relapses is not essentially different 
from that of the primary attack. The prognosis in children, as a rule, 
is good. 

Treatment. — In typhoid fever probably as much as, if not more than, 
in any other disease, our duty is not to our patient alone, but in a special 
sense to the community at large Since typhoid fever is a preventable 
disease, it should be prevented; the duty of preventing it falls upon 
the physician no less than upon the public health authorities. The 
general measures of prophylaxis set forth on page 29 should be 
scrupulously followed. 

Whether Wright's preventive inoculation will ultimately commend 
itself to the profession is at least doubtful. According to British 
army surgeons, typhoid fever is more than two and a half times as 
common, and one and a half time as fatal, among the uninoculated 
as compared with the inoculated troops. Of possible value during 
times of war, inoculation is not likely soon to attain much vogue in civil 
practice; it may prove of service among hospital attendants. The serum 
treatment of the disease, for which Chantemesse and others claim good 
results, has not commended itself to the profession at large. A satis- 
factory vaccine (bacterin) treatment has not yet been devised. 

Since typhoid fever is a self-limited infection, the special function of 
the physician is to assist, never thwart, the well-directed efforts of 



TYPHOID FEVER 51 

nature. This comprises attention to, (1) the general management of 
the patient, (2) the diet, (3) hydrotherapy, and (4) medicinal and 
otGer measures indicated symptomatically. 

General Management. — Whether the patient shall be treated in 
his home or in a hospital is a matter to be decided in each individual 
case ; in general the hospital patient has the advantage, since the nursing, 
as a rule, is better and the necessary manipulations can be more easily 
carried out; disinfection is more thoroughly practised; complications 
are likely to be sooner recognized (since a physician is always at hand) ; 
and in the event of surgical intervention being necessary, it can be 
undertaken sooner and under better auspices than in the patient's home. 
But under proper supervision, the patient may be very well treated at 
his home. Under all circumstances, he should be isolated — in the 
hospital, in a ward or room set apart for this purpose; at home, in a 
room affording abundance of sunlight and fresh air. He should be 
confined absolutely to bed until he is well along in convalescence, and 
he must use a bed-pan and a urinal. Special attention should be 
directed to avoiding creases in the bed-linen so as to promote the comfort 
of the patient and prevent, as far as possible, the development of bed 
sores. The patient should be turned on his side from time to time, and 
his skin, especially of the back, should be frequently sponged with 
dilute alcohol (50 per cent.) or with equal parts of alcohol and alum 
water; following this a drying powder may be applied, such as zinc 
stearate, or equal parts of powdered zinc oxide and boric acid. Should 
the skin become irritated, one may substitute a mixture consisting of 
boric acid 10 grains (0.65 gram), zinc oxide 1 to 2 drams (4 to 8 grams), 
and castor oil 1 ounce (30 grams) . The mouth and throat should be 
kept clean and sweet by the use of mild antiseptic solutions, such as 
boric acid (3 per cent.) ; or boric acid (1 dram, 4 grams), glycerin (6 drams, 
25 grams) , and rose water (6 ounces, 200 grams) ; or liquor antisepticus 
(U. S. P.); or the following: 



1$ — Carbolic acid 6 minims 

Oil of eucalyptus 10 minims 

Sodium borate 1 dram 4 

Glycerin 3 drams 12 

Distilled watsr, sufficient to make ... 3 ounces 100 



40 
60 
00 
00 
00.— M. 



The physician should always write his orders in detail, rather than 
trust to the memory of even a well-trained nurse; in the absence of a 
trained nurse, this is all the more imperative. 

The general management of convalescence often demands much 
tact on the part of the physician — to withstand the importunities of the 
patient and the usually well-meant, but often ill-advised, endeavors of 
his solicitous friends. Could solicitous friends be banished for a while, 
most typhoid-fever patients would fare better; at all events, the visits 
should be as short as possible, and all matters that may excite the patient 



52 BACTERIAL INFECTIONS 

or disturb his emotions should be scrupulously avoided. On the fifth or 
the sixth day of normal temperature, in the ordinary case, the patient 
may be propped up in bed for a while, and on the eighth day or there- 
abouts he may sit in a chair. A general tonic is usually advantageous, 
though often not necessary; anemia, however, calls for the administra- 
tion of iron. Return to ordinary avocations should be postponed 
as long as possible, especially after severe infections; return to mental 
work and study, in particular, should be delayed, since a too early 
return not infrequently results in a prolonged spell of cerebral asthenia. 
A sea voyage subserves a most useful purpose following convalescence. 

Diet. — The diet should be suited to the individual patient, rather 
than to the disease. The physician should remember that during 
typhoid fever the digestive juices are lessened or perverted, and that 
some at least of the toxemia is due to the poisonous effects of the end- 
products of destructive katabolism of the body protein; and while he 
should endeavor as far as possible to supply a sufficiency of calories in 
foodstuffs to satisfy dynamic needs and to minimize loss of weight, he 
must be careful to avoid improper food and that excess of food which is 
certainly productive of digestive disorders. If in the past we have 
been perhaps too much committed to a diet insufficient in calories and 
relatively too rich in protein, a diet of too high caloric value may be 
productive of much harm; certain carbohydrates, under circumstances, 
may be of value; fats, at least in excess, are not well borne. In many 
respects the appetite is a good index of the amount, although not of the 
character of the food that may be permitted. 

There can be no doubt that at present, as in the past, the majority of 
patients do best on a diet consisting largely, if not wholly, of milk. To 
an adult one may give four, six, or eight ounces of milk every two hours 
during the day, and every four hours at night — nine or ten feedings in 
the twenty-four hours. This furnishes from 780 to 1750 calories 
(650 to 700 calories to a quart or liter). The milk may be given hot 
or cold; it may be diluted with lime water or some carbonated water, 
such as Vichy; it may be flavored with salt, vanilla, coffee, tea, cocoa, 
or port or sherry wine; or it may be given as buttermilk, koumiss, 
matzoon, junket, or in part as ice cream. Twice a day, the white of an 
egg (20 calories) or the whole egg (80 calories) , if well borne, may be 
added to the milk. In case of objection on the part of the patient, 
albumen water (the whites of two eggs added to four to six ounces of 
water, and flavored with lemon, lime, or orange juice) may be substituted 
for the milk at every other feeding. In ordinary cases, throughout the 
febrile period, I commonly adhere to this diet of milk and egg-albumen 
— the advantage of which is seen in the freedom from intestinal dis- 
orders, the good general condition of the patient, and the usually prompt . 
convalescence without noteworthy untoward symptoms. However, in 
the event of very serious objection to milk on the part of the patient, or an 
obvious poor general condition, I have no hesitation in substituting the 
milk in whole or in part, or adding to it, cream, milk sugar, eggs, meat and 



TYPHOID FEVER 53 

vegetable soups 1 strained and thickened with flour, powdered rice or 
barley, cream, egg, etc., or strained oatmeal gruel, cornstarch, arrow-root, 
potato puree, gelatine flavored with wine, etc. 

In the event of tympanites or diarrhoea, the milk should be reduced in 
amount; usually, under these circumstances, too much rather than too 
little is being given, and curds frequently appear in the stools. Whey, 
boiled milk, peptonized or pancreatized milk, or koumiss may be substi- 
tuted; but if the unfavorable symptoms do not subside promptly the 
milk should be entirely withheld for twenty-four to thirty-six hours, 
and albumen water given instead. Thereafter one may cautiously 
recommence with peptonized milk in small amounts, or resort to some 
of the other mentioned foodstuffs. If the patient has done well on the 
milk and egg-albumen dietary, toward the end of the third week, in the 
absence of definite indications to the contrary, two raw eggs daily should 
be added to the diet ; and during the following week, the aforementioned 
gruels, broths, soups, cornstarch, etc., as well as very soft-boiled eggs. 
At the end of four to seven days of normal temperature, soft puddings, 
milk toast, scraped beef, mashed potato, apple sauce, etc., may be 
allowed ; and a day or two later, sweetbreads, the white meat of chicken, 
stewed fruit, etc. The return to the ordinary diet should be gradual. 
Thus, while I incline to liberality in the matter of diet, especially toward 
the end of the disease, I have jet to see any general good come from the 
unusually generous dietary, even solid food, sometimes advocated, and 
I have seen it do positive harm. 

Of quite as much importance as food is water. A minimum of 
three or four liters, in stated amounts between the feedings, should be 
given in the twenty-four hours; often much more can be taken with 
great advantage to the patient. The daily amount of urine is the best 
indication of the amount of water that should be given, and we may 
be sure that that patient who passes eighty, one hundred, or more 
ounces of urine daily will recover unless he suffers a severe hemor- 
rhage or a perforation. 

Hydrotherapy. — Hydrotherapy constitutes an essential part of the 
treatment of every typhoid-fever patient. Advocated originally by 
Currie, of England, hydrotherapy was systematized in 1861, and sub- 
sequently, by Brand, and is commonly known as the Brand treatment. 
Its advantages are many, the most important of which is not the 
reduction in temperature which it effects. Its greatest claim to our 
attention is that it unquestionably reduces the mortality — large statistics 
showing undoubtedly that from five to seven of every one hundred 

1 Houghton gives the following formula for the preparation of a vegetable soup: 60 grams 
(2 ounces) each of green or canned French peas, white dry beans, potato, rice, and noodles, and 
15 grams (H ounce) of carrot, should be boiled in water for at least four hours. Thereupon 
sufficient water should be added to make one liter (1 quart), which is sufficient for four feedings. 
This yields 760 calories, of which 6.3 per cent, is protein, 43.9 per cent, carbohydrate, and less 
than 0.2 per cent. fat. When ready to use, the sediment should be stirred up, and the patient 
allowed to eat everything except the pea- and bean-skins. Onion may be added for flavoring, 
if desired. 



54 BACTERIAL INFECTIONS 

typhoid-fever patients are saved by its use. The patients saved are not 
the unfortunate subjects of complications such as hemorrhage and 
perforation, but patients who otherwise would die of toxemia. Hydro- 
therapy, therefore, does good by reducing toxemia, and largely through 
an influence on the nervous system. 

Although, for obvious reasons, the degree of temperature is taken as 
the indication for repeating the hydrotherapeutic measures, the influence 
of the bath on the fever, especially during the fastigium, is often com- 
paratively slight, though the toxemia may be notably influenced. Com- 
monly, however, more or less bodily heat is abstracted; reduction of the 
temperature of from 2° to 4° after the baths is frequent, especially after 
the treatment has been in use for several days ; and the ill effects of long- 
continued fever are obviated. The notable influence, however, is on 
the toxemia : the nervous manifestations of the toxemia, mental dulness, 
stupor, delirium, muscular twitchings, etc., are much improved, the 
" typhoid state" of our forefathers is rarely seen in patients subjected 
to the bath treatment from the beginning, and insomnia and coma vigil 
when present often after a bath give way to several hours of refreshing 
sleep ; the toxic weakness of the heart and circulation (low blood pressure) 
is replaced by fuller, slower, and stronger heart beats, the blood pressure 
is increased, and peripheral cyanosis, hypostatic congestion of the lungs, 
venous thromboses, and other ill consequences of low blood pressure 
are warded off; shallow breathing gives way to full and deep inspirations, 
the cyanosis of ill-ventilation is lessened, the good results of improved 
oxygenation are obtained, and the bronchitis is improved, whence the 
likelihood of bronchopneumonia is lessened; the kidneys are stimulated 
to increased functional activity, and typhotoxins are excreted in in- 
creased amount; and the invigorating action of the baths and friction on 
the skin and the cutaneous capillaries improves the general tone of the 
system and diminishes the likelihood of bed sores. 

Objections to the cold-bath treatment are: that it is troublesome 
— which is true, especially in private homes ; that it is attended by no 
better results than other forms of treatment — which is not true; that it 
increases the likelihood of hemorrhage and perforation — which is not true, 
although certain series of cases may show somewhat higher percentage 
incidence of these complications: they show also a higher percentage 
of recoveries; that it is cruel, inhuman, and barbarous — which contains 
an apparent modicum of truth, but in reality the treatment does not add 
notably to, in many respects it reduces, the discomfort of the attack of 
typhoid fever, and assuredly it is better to suffer the ills of two or three 
weeks of cold-bath treatment than fly to those we know not of; and that 
it is not necessary in all cases — but the good results of the treatment are 
seen to best advantage only when it is instituted early and continued 
systematically throughout the attack, and not when postponed until 
the patient is "sick enough," a practice that unfortunately still obtains 
among some practitioners. No one can foretell at the beginning of an 
attack how severe it is likely to become. 



TYPHOID FEVER 55 

The hydrotherapeutic measures to be commended in typhoid fever 
are the cold bath and sponging; the cold pack, sprinkling, and fanning 
are more or less unsatisfactory substitutes — available, however, in some 
cases. 

The cold bath is the most preferable and is in general use in most 
modern hospitals, and as far as circumstances will permit is largely used 
by many physicians in their private practice. The common practice is 
to give the patient a bath at 70° F., for fifteen or twenty minutes, every 
three hours, if his temperature reaches or is above 102.5° F. While in 
the water, the patient's body should be submerged, a cold cloth or an 
ice-bag should be applied to his head, the exposed neck, shoulders, and 
chest should be douched repeatedly with cold water, and his extremities, 
back, and chest should be rubbed vigorously and continuously — an 
essential of the treatment. At the termination of the bath the 
patient should be wrapped in a dry, preferably warmed, sheet (pre- 
viously, with a blanket, spread upon the bed); the sheet should be care- 
fully tucked about the patient's extremities and trunk, and gentle friction 
made to remove the excess of water; hot-water bottles may be applied 
to his feet and legs, and then he should be covered with the blanket. 
After the patient is dry, the sheet may be removed and the patient 
allowed to rest in the blanket for twenty to thirty minutes, whereupon 
a dry nightdress should be provided. The rectal temperature should 
be taken at the termination of the bath, and again at the end of a 
half-hour. Usually a fall of temperature of from 1° to 2° will have 
been attained; this is sufficient, marked falls (4° and thereabouts) being 
undesirable. 

Certain deviations from this strict regimen are not only permissible, 
but often desirable — due attention being paid to the patient rather than 
to the disease. Thus, it is by no means necessary that the water should 
be always at 70° F.; it may vary from 70° to 85° F., and it is often desir- 
able to begin with a temperature of 85° F. in adults, and sometimes to con- 
tinue with this temperature throughout the attack in children. Beginning 
with 85° in apprehensive adults, the temperature may be reduced 5° 
while the patient is in the bath, by the addition of ice or cold water — the 
cold water being preferable, since it is less likely to add to the appre- 
hensiveness of the patient. Each succeeding or every second bath may 
begin at a temperature of 5° less, until the desired and the best tempera- 
ture for the particular patient is obtained. Some patients, however, 
never do well with a temperature as low as 70° F. It is usually desirable 
to have the first bath last not more than five or ten minutes and gradually 
to lengthen the time of succeeding baths until the desired fifteen or twenty 
minutes is attained. 

While in the bath some patients complain much of the low temperature; 
others shiver much, their teeth chatter, and they become more or less 
cyanosed; while others do not complain at all. Much depends upon the 
skill and tact with which the bath is given. Brand originally recom- 
mended that a glass of red wine be given the patient before and after 



56 BACTERIAL INFECTIONS 

the bath; whiskey has been largely substituted in this country, but it 
is not necessary as a routine measure. In the event of unusual shivering 
or of cyanosis, especially of the face (rather than of the extremities, 
which occurs in practically all patients), a half-ounce (15 c.c.) of whiskey 
may be given; but equally good results attend the use of hot coffee, 
hot broth or milk, aromatic spirit of ammonia, Hoffmann's anodyne, 
etc. The patient should be removed immediately from the bath upon 
the occurrence of marked cyanosis (especially of the face), cardiac col- 
lapse, acute abdominal pain, vomiting, or intestinal hemorrhage. The 
baths are contraindicated in the event of severe abdominal pain, 
hemorrhage, perforation (peritonitis), cholecystitis, thrombophlebitis, 
unusual prostration, and cardiac weakness. 

More than six tub baths are rarely required in the twenty-four hours. 
The patient should be allowed, if he will, to sleep at night; should 
the temperature be unusually high, cold sponging may be substituted 
for the bath at night. Following the suggestion of Dr. John H. Musser, 
I have been in the habit, for a number of years, of giving a tub bath for 
fifteen minutes when the temperature is above 103° F., and a sponge 
bath when the temperature is above 102° F. ; thus while the treatments 
are increased in number, the number of tub baths, especially troublesome 
in private practice, are reduced. Various portable bath-tubs have been 
devised for use in private practice. 

Cold sponging is an alternative hydrotherapeutic measure often 
necessary in private practice, and sometimes advisable in children and 
elderly persons. The water may be at 70° F., or less, even ice water, 
depending upon the indications in the case and the reaction of the 
patient. The general indications, and the frequency and duration of the 
spongings, are similar to those of the tub baths. While it is best to 
expose only that of the body being sponged, the patient should not be 
dried until the process is completed, since to insure reduction of the 
temperature a layer of water must be provided for evaporation. 

The cold pack is sometimes serviceable in children. The patient should 
be wrapped in a sheet (previously doubled and wrung out of water at 
60° to 70° F.), and then covered with a blanket — where he may remain 
for from thirty minutes to an hour. The patient sometimes sweats 
considerably, and the temperature may be reduced a degree or two; 
but the reaction and the influence on the toxic and nervous symptoms 
are, as a rule, not so marked as after the cold tub bath. Sprinkling the 
patient with cold water from a watering-pot, or by means of a spray- 
nozzle attached to an irrigating reservoir, is also efficacious in some cases. 
Evaporation may be facilitated by fanning the patient after the applica- 
tion of a wet sheet, which may be sprinkled from time to time. The 
application of continuous cold to the abdomen by means of an ice-bag 
or a Leiter's coil is favored by some practitioners, who believe that it 
reduces the temperature and lessens the likelihood of intestinal hemor- 
rhage and tympanites. If none of the foregoing measures is resorted 
to systematically, the patient should be bathed at least once, prefer- 



TYPHOID FEVER 57 

ably twice, daily, merely as a matter of cleanliness, to prevent bed sores, 
and to equalize the circulation. 

Medicine. — Medicines should be given only when clearly indicated. 
I believe it good practice, though often not necessary, following ancient 
custom, if the patient comes under observation before the tenth day, 
and especially in the event of constipation, to give an aperient dose of 
blue mass (5 grains, 0.3 gram) or of calomel (5 to 10 grains at one dose, 
or J grain, 0.008 gram, every fifteen minutes for eight doses), followed by 
an enema or a saline cathartic. In view of the common deficiency of 
gastric juice, and the occurrence of a dry, brown,, coated tongue, it is 
advisable, especially in private practice, to give 10 to 15 minims (0.6 
to 1 c.c.) of dilute hydrochloric acid, three times daily. Aside from 
this, many patients may require no medicine throughout the entire 
course of the disease. 

The so-called intestinal antiseptics are of little use, since they do not 
achieve the object for which they are intended (the harmful bacteria 
are not those in the lumen of the intestine, but those in the lymphatic 
and the blood streams); they sometimes do some good, however, in 
preventing or limiting tympanites. The best is probably salol, which I 
believe I have seen do good. I have rarely seen any indication for ad- 
ministering carbolic acid, the mercurials, iodine, /?-naphthol, menthol, 
thymol, guaiacol, chlorine, acetozone, etc. Those who desire only to 
reduce the temperature may use guaiacol, 30 minims (2 c.c), painted 
on the skin of the abdomen and flank. Since I have never used any 
of the coal-tar antipyretics, except in an occasional dose, in the early 
stages of the disease, to relieve headache or severe neuromuscular 
pains, I am happy in the conviction that I have avoided doing my 
patients considerable, sometimes even fatal, harm — of which these 
drugs are unquestionably capable. 

Alcohol should not be used as a routine measure, but should be with- 
held until it is clearly indicated, when without doubt it" does considerable 
good. When the pulse becomes weak and dicrotic, the first sound of the 
heart weak and valvular; when insomnia is persistent and the fever high; 
and when the typhoid state develops, alcohol renders excellent service. 
It should be given carefully and not in too large amounts — beginning 
with a half ounce three or four times daily. In some cases the poor 
condition of the patient is due largely to the amount of alcohol given, 
and improvement immediately follows its discontinuance. Headache, 
in the early stages, is usually relieved by an ice-bag, sodium bromide, or 
a small dose of codeine or morphine; rarely one of the coal-tar deriva- 
tives, such as acetphenetidin or acetanilide, may be given in small doses, 
but a few doses only. Insomnia is best relieved by hydrotherapeutic 
measures, the patient not infrequently enjoying a refreshing sleep after 
the baths. General restlessness, particularly at night, is best controlled 
by a Dover's powder or a small dose of morphine hypodermicly. The 
bromides, codeine, chloralamide, trional, sulfonal, and similar remedies 
are sometimes useful. 



58 BACTERIAL INFECTIONS 

Delirium and other manifestations of severe intoxication are best con- 
trolled by hydrotherapeutic measures. An ice-bag should be kept to 
the head continuously. Alcohol is useful, and is often required in rela- 
tively large amounts, but the caution already mentioned should be 
heeded. With the development of the typhoid state, stimulation must 
be more active, and special efforts must be made to rid the patient of 
toxins. Water should be given in very large amounts, and hot enteroc- 
lysis and hypodermoclysis (0.9 per cent, saline solution) are extremely 
serviceable. Cocaine, camphor, and codeine hypodermicly often con- 
trol markedly the mental wandering, the carphologia, and the subsultus 
tendinum. Strychnine (^ to -^ grain; 0.0015 to 0.003 gram) is often 
of value, but it should not be given continuously, since it often tends to 
aggravate the condition. In cases of marked cardiac asthenia with low 
blood pressure, the addition to the saline solution by hypodermoclysis 
of 2 to 4 c.c. of adrenalin chloride is often followed by good results. 
Digitalin germanicum (Merck), y 1 ^ to J grain (0.005 to 0.01 gram) 
hypodermicly, also often seems to do good, although it is said to lose 
much of its efficiency during states of fever. The meningism that 
much simulates meningitis is often markedly relieved by lumbar 
puncture. 

Constipation rarely requires much treatment, and constipation as 
such is much to be preferred to diarrhoea. A simple soap-suds enema 
or an oil enema should be given every other day if the bowels do not 
move spontaneously. During the height of the disease no purgatives 
whatever should be given by the mouth. During convalescence special 
attention should be paid to the bowels, since, despite a daily evacuation, 
even of liquid feces, the patient may be constipated; that is, his rectum 
and colon may be more or less filled with hardened feces. The rectum, 
the urinary bladder, and the gall-bladder should be the special objects 
of concern in delayed convalescence. Well on in convalescence castor 
oil often subserves a useful purpose. 

Diarrhoea should not be checked unceremoniously, not unless there 
are more than four movements in the twenty-four hours, and they are 
distressing and weakening to the patient. Since ill-digested food is 
usually the cause, the milk should be stopped, temporarily at least, and 
albumen water substituted. Bismuth, salol, and chalk mixture, or a lead 
and opium pill, or aromatic sulphuric acid and other astringents, may be 
administered for a few days, but care should be exercised that scybalous 
masses do not form. Tympanites, often associated with diarrhoea, is by 
no means so common as in the days prior to the cold-bath treatment. 
When developed it may usually be controlled by withholding the milk, 
temporarily at least, and administering turpentine externally (hot stupes), 
by the mouth, and by the rectum, if necessary. Charcoal, resorcin, 
/2-naphthol, zinc sulphocarbolate, etc., by the mouth, and milk of 
asafcetida, by the rectum, are also sometimes of service. A rectal tube 
may be inserted high up in the sigmoid. A hypodermic injection of 
eserine ( t ^q- to ^ grain, 0.0006 to 0.C013 gram) is sometimes efficacious 



TYPHOID FEVER 59 

in causing the expulsion of considerable gas. Vomiting is rarely severe, 
and when present is usually controlled by withholding food for a time, 
and giving lime water with creosote or carbolic acid (in % grain, 0.008 
gram, doses), bismuth, cerium oxalate, sips of hot water, brandy, or dry 
champagne. Hot applications to the abdomen are also of service. 

Hemorrhage is best treated by securing absolute rest to the patient 
and his intestines — by disturbing the patient as little as possible, even 
for evacuating his bowels, withholding all food for at least ten or twelve 
hours, and giving morphine hypodermicly. An ice-bag may be applied 
to the abdomen, except in the event of marked collapse and lowered 
temperature; custom sanctions the use of ice internally. How long 
the morphine should be continued must be determined in individual 
cases — remembering that, though it inhibits peristalsis, it favors intestinal 
distention, and in the event of perforation (associated in from 15 to 20 
per cent, of the cases of hemorrhage) it masks the symptoms and may 
prevent their recognition. Turpentine is recommended to control re- 
peated oozings. I have never seen undoubted good follow the use of 
any of the styptics, but lead (in the well-known lead and opium pill), 
Monsel's solution of iron sulphate, tannic acid, etc., may be used by 
those committed to the practice. Calcium chloride seems indicated 
theoretically to promote the coagulation of the blood, but its effects 
are lost after several days' use. Gelatine has largely gone out of 
use hypodermicly, but it may be given by the mouth, especially when 
food is recommenced, in the hope that it will favor the coagulation of 
the blood; but its action is at least doubtful. In the event of collapse, 
the foot of the bed should be elevated, hot-water bags should be applied 
about the patient, and hypodermoclysis and diffusible stimulants, such 
as ether and camphor, should be administered. Recently operation 
has been advised to control severe bleeding. 

Perforation and peritonitis (which may be due to causes other than 
perforation) calls for immediate operation — now-a-days done largely 
under local anesthesia. The mortality without operation is at least 
95 to 98 per cent., an occasional patient seeming to recover without 
operation, but in such cases the diagnosis must always remain more 
or less in doubt. With improved technique and early operation the 
mortality is becoming less and less, and is now probably not more than 
60 to 65 per cent. ; that is from 30 to 35 per cent, of patients are saved 
who otherwise would inevitably perish. Without operation, the treat- 
ment consists of supportive measures: opium to relieve pain, and hot 
water bottles, hypodermoclysis, and stimulants to combat shock and 
peritoneal sepsis. 

Cholecystitis usually subsides without untoward symptoms, though it 
is usually the first of a train of serious symptoms (gallstones, etc.) that 
may develop in later life. If the symptoms are acute, however, if 
they increase rather than subside, and especially if there is reason to 
suspect suppuration or perforation, operation should be undertaken. 
In all cases the patient must be under continuous competent observa- 



60 BACTERIAL INFECTIONS 

tion, so that should operation be called for it may be undertaken without 
delay. There is much to commend operation following recovery with 
a view to prevent the later development of gallstones. 

Bed sores are better prevented than cured. Perfect cleanliness is 
imperative; the bed-linen should be well cared for and creases pre- 
vented; the patient should be turned frequently from side to side, and 
he should be bathed frequently with alcohol, alum water, etc.; and 
should any redness develop he should be placed upon an air cushion, 
and the reddened area painted with a 5 per cent, silver nitrate solution. 
If a bed sore develops, all pressure must be removed, by the use of 
the air-cushion, pads, or a water-bed or an air-bed; the ulcer should 
be treated antiseptically and with a drying dusting powder consisting of 
boric acid, zinc steorate, and bismuth subnitrate; all dead tissue 
should be removed, and if the granulations are sluggish, stimulating 
applications of silver nitrate should be made. 

Thrombosis of the femoral or other veins should be treated by rest of 
the limb in an elevated position, and the application of cotton wool, 
an ichthyol ointment (33 per cent.), a lead and opium lotion, or a 
saturated solution of magnesium sulphate. In the early days an ice-bag 
over the thrombosis will relieve the pain. Later, mercury, belladonna, 
and iodine ointment (equal parts) is useful, but rough handling must 
be avoided on account of the possibility of embolism. Tender toes 
(peripheral neuritis) may be relieved by alcohol rubbings, massage, 
counterirritation (iodine, etc.), ichthyol ointment, and aconitine oint- 
ment (2 per cent.). Bacilluria, a frequent and unsuspected source of 
infection, is usually controlled by hexamethylenamine, 10 to 15 grains 
(0.6 to 1 gram) three times daily. It is advisable to give this as a 
routine measure for four or five days in the early days of convalescence. 
Should cystitis develop, we may use, in addition to the hexamethylena- 
mine, irrigations of the bladder with mercuric bichloride, 1 to 50,000. 
As previously stated, the urine of every typhoid-fever patient should 
be disinfected. 



PARATYPHOID FEVER. 

Paratyphoid fever is an acute infectious disease caused by Bacillus 
paratyphosus (Archard and Bensaude); clinically it is characterized 
by symptoms that do not distinguish it from typhoid fever. 

Etiology. — The term Bacillus paratyphosus is used as a convenient 
designation for a group of bacilli intermediate in biological type between 
the typhoid and the colon groups. Of the many subdivisions of these 
organisms, one much resembles Bacillus typhosus, another Bacillus coli, 
while others exhibit biological characteristics pertaining to Bacillus 
enteritidis, Gartner (the meat poisoning bacillus), Bacillus suipestifer 
(hog cholera), and Bacillus psittacosis. Following Schottmuller and 
Buxton the paratyphoid bacilli are commonly divided into: (1) The 
paracolon bacilli, a group of organisms differing somewhat among 



PYOGENIC INFECTIONS 61 

themselves but culturally very much alike, and, as a rule, not causing 
typhoid-fever symptoms in man; and (2) the paratyphoid bacilli, a 
group of organisms that do cause typhoid fever in man and are sub- 
divided into Bacillus paratyphosus a, distinctly unlike the paracolon 
bacilli, and Bacillus paratyphosus /?, resembling the paracolons, but a 
distinct species. Bacillus coli and Bacillus fsecalis alcaligenes also seem 
to be capable of causing a typhoid-like infection, so that the term 
typhoidal disorders is sometimes used to include this whole group of 
diseases. Aside from the specific cause, the etiological factors of para- 
typhoid fever are similar to those of typhoid fever. 

Pathology. — The disease is a general bacteremia, and local lesions 
may be inconspicuous or entirely absent. The common noteworthy 
lesion is enlargement of the spleen. Otherwise the disorder resembles 
most of the bacteremias. The characteristic lesions of typhoid fever 
are usually absent; Peyer's patches and the solitary glands are slightly 
if at all altered; intestinal ulceration, in the few cases observed, has 
resembled dysenteric rather than typhoid ulceration ; proliferative changes 
in the endothelium and endothelial phagocytosis, so characteristic of 
typhoid fever, have not been observed. Doubtless, many of the cases 
of so-called typhoid fever without intestinal lesions have been examples 
of paratyphoid infection. 

Symptoms. — In general the symptoms are those of typhoid fever, but 
as a rule, paratyphoid fever has a shorter period of invasion, and the 
fever is less high, exhibits more marked diurnal variations, has a shorter 
course (twelve to twenty days), and ends rather rapidly (crisis or rapid 
lysis). Prolonged (eighty-four day), severe, and even fatal cases, 
however, have been observed. Diarrhoea appears to be somewhat 
more common than in typhoid fever. Intestinal hemorrhage occurs in 
from 5 to 10 per cent, of the cases. Pratt has emphasized the frequency 
of complications — which are often purulent in character. Relapses are 
about as frequent as in typhoid fever. 

Diagnosis. — The disease is usually suspected to be typhoid fever 
until the Gruber-Widal reaction with the typhoid bacillus is found to be 
absent. The diagnosis depends then upon the recovery of the infecting 
microorganism — from the blood, the spleen, the urine, the feces, the 
sputum, the rose-spots, or the complicating lesions; or the diagnosis 
may be made by the agglutination reaction with known strands of 
paratyphoid bacilli. 

Prognosis. — The mortality is low — not more than 3 per cent. 

Treatment. — The treatment is similar to that of typhoid fever. 

PYOGENIC INFECTIONS. 

(Pyococcic Infections; Septic Infections; Sapremia; Septicemia; Pyemia; 
Septicopyemia; Toxemia; Bacteremia.) 

The pyogenic infections comprise a group of non-specific infectious 
diseases, some local and some general, caused by the different pyogenic 



62 BACTERIAL INFECTIONS 

microorganisms, and characterized by fever, leukocytosis, a variable 
degree of systemic intoxication, sometimes by bacteremia, chills, and 
sweats, and often by at least a local focus of inflammation or suppuration. 

Etiology. — The pyogenic infections occur in all parts of the world 
and at all seasons; they are common at all ages, and under like conditions 
they affect the sexes equally — but for very obvious reasons women alone 
suffer from that form known as puerperal infection. While the robust 
are by means immune, these infections are especially common in persons 
debilitated from any cause, and they are often the terminal event in the 
course of many other diseases (terminal infections). 

The exciting causes of these infections are especially the pyogenic 
cocci — Staphylococcus pyogenes aureus (citreus et albus), Streptococcus 
pyogenes, Diplococcus pneumoniae, Micrococcus gonorrhoea, Micro- 
coccus intracellulars meningitidis, and Micrococcus tetragenus. Many 
bacilli and certain streptothrix also give rise to pyogenic infections, 
of which the more important are Bacillus coli communis, Bacillus 
typhosus, Bacillus pyocyaneus, Bacillus aerogenes capsulatus, Bacillus 
tuberculosis, Bacillus anthracis, Bacillus mallei, Bacillus pestis, and 
Friedlander's pneumobacillus. Although these bacilli unquestionably 
may produce suppuration, the pyococci are not infrequently associ- 
ated with them, as well as with other bacilli (the diphtheria bacillus, for 
instance); that is, mixed infections are quite common. Infection may 
be transmitted by direct inoculation (such as infected sutures at opera- 
tion), contact (such as necropsy and dissection wounds), or proximity 
(infected wounds and gangrene in hospitals and other infected localities), 
by a third person, and by fomites of all kinds. Susceptibility to the in- 
fection is much enhanced by a wound, abrasion, or traumatism of the 
skin or mucous membrane ; in fact, were it not for the protection afforded 
by the skin and the mucous membranes these infections would be much 
more common than they are, since pathogenic staphylococci and often 
streptococci may readily be cultivated from the skin and certain mucous 
surfaces of the most human beings and lower animals, and they abound 
in the air, dust, and soil about us. Infection may be acquired by inhala- 
tion or ingestion, but it is much more commonly acquired by direct inocu- 
lation into the blood stream or the lymph stream (through a wound or 
abraded surface). 

Pathology. — These pyogenic infections still labor under the embar- 
rassment of descriptive terms born of ignorance and perpetuated in this 
day of comparative enlightenment — such as sapremia, septicemia, and 
pyemia. Sapremia was understood to be a condition due to poisoning 
by the chemical products of bacteria, but unattended by the entrance of 
the bacteria themselves into the blood; septicemia (septic infection, 
putrid material in the blood) was a condition due to the growth and 
development of microorganisms in the circulating blood, as well as to 
poisoning by their chemical products; and pyemia (pus in the blood), 
also called septicopyemia, comprised in addition to the foregoing the 
development of multiple abscesses in different parts of the body. And 



PYOGENIC INFECTIONS 63 

when the source of the infection was not discoverable the condition was 
spoken of as cryptogenetic. These distinctions, however, are strained 
and artificial: except when introduced intentionally or taken in certain 
forms of food poisoning, poisoning of the body by the products of bacteria 
cannot occur independently of the presence of bacteria in the body, and 
contrary to former opinions, we now know that bacteria enter and circulate 
in the blood stream much more frequently than was formerly supposed, 
and that abrasions and other small and inconspicuous wounds of the 
skin and mucous membranes are frequently the infectious atria of what 
formerly would have been regarded as cryptogenetic sepsis or infection. 
Since, therefore, it is impossible, clinically as well as anatomically, to 
separate the one of these conditions from the others, since in reality they 
are but stages of the one process, it is much preferable to speak of them 
as pyococcic (or other) infections; when possible to qualify these by 
adjectives such as staphylococcic, streptococcic, pneumococcic, gono- 
coccic, etc. ; and to use the terms toxemia and bacteremia in their very 
obvious meanings. It is desirable to bear in mind also that it is usually 
impossible to distinguish between bacterial intoxication and bacteremia. 

The pyogenic infections may be classified as follows : (1) Local infec- 
tions; (2) general infections (a) with and (b) without obvious infectious 
atria; and (3) terminal or secondary infections. 

Local Infections. — The local infections provoked by pyogenic 
microorganisms, especially staphylococci and streptococci, are legion, 
and comprise the inflammatory processes which arise in all parts of the 
body and which may or may not progress to suppuration, such as fur- 
uncle, carbuncle, abscess, phlegmon, cellulitis, erysipelas, lymphangitis, 
phlebitis, bronchitis, pleuritis, pericarditis, endocarditis, peritonitis, 
appendicitis, cholangitis, salpingitis, osteomyelitis, arthritis, puerperal 
infection, etc. As long as these (and other) infections remain local, the 
systemic intoxication is due solely to the soluble toxins produced by 
the bacteria and absorbed into the lymphatic and blood streams; in 
this respect these infections resemble certain specific infections, 
such as diphtheria and tetanus, in which the systemic symptoms are 
toxic solely. The severity of the symptoms, the toxemia, is proportionate 
to the amount and virulence of toxins absorbed, and since the toxin 
is being constantly excreted, especially by the kidneys, removal of the 
toxin-producing focus, such as a putrescent placenta, a pelvic abscess, 
an empyema, etc., results in almost immediate lessening of the toxic 
manifestations, and unless irreparable damage has already been done, 
recovery usually ensues. Contrary to former opinions, we now know 
that in many of these local infections there is a disposition to an early 
invasion of the lymphatic and blood streams, whence to the toxemia 
bacteremia is added. The bactericidal properties of the blood serum, 
however, are considerable, and though invasion of the blood may occur, 
general infection is often prevented. 

General Infections. — Frequently on account of the virulence of the 
invading microorganisms the bactericidal properties of the blood are 



64 BACTERIAL INFECTIONS 

overcome and general infection (bacteremia) occurs. This may or 
may not be associated with multiple abscess formation, whence it is 
spoken of as septicemia or pyemia, respectively. The term septicemia 
is also employed to designate the bacteremia that sometimes occurs in 
other infections, such as typhoid fever (typhoid septicemia), gonococcic 
infection, anthrax, etc. 

These general infections may occur with or without an obvious local 
lesion. Much interest attaches to those cases, by no means rare, in 
which no local infection can be found during life or after death — 
so-called cryptogenetic infection or septicemia. Diligent search often 
results in the discovery of a small local lesion that otherwise would 
have gone undetected, but in some cases the most rigorous investigation 
fails to reveal any local source of infection. In the majority of cases, 
however, general infection is preceded by some local lesion, inconspicu- 
ous or apparently insignificant though it may apparently be, such as an 
acne pustule, a furuncle, a stitch abscess, a small abrasion; a latent or 
masked osteomyelitis, otitis media, adenitis, empyema, cholecystitis, or 
appendicitis; an unsuspected abortion, retained placenta, etc. Infection 
may be transmitted: (1) Along the lymphatics (which may or may not 
become actively inflamed); (2) by way of the venous circulation, in 
which event the venules frequently, and the larger veins sometimes, 
become thrombosed ; and (3) sometimes by way of the arterial stream, 
especially in pulmonary or endocarditic lesions, or, as rarely happens, 
when a local focus of suppuration ruptures directly into an artery. 
Should the venous thrombi soften (a rather common event), the emboli 
carried to different parts of the body act either mechanically, producing 
infarction, or, if they contain virulent bacteria, setting up disseminated 
foci of suppuration: metastatic or embolic abscesses (so-called pyemia, 
or septicopyemia). Similar results ensue if the infectious matter is 
transported by the arterial stream. These metastatic phenomena occur 
especially: (1) In the lungs, particularly when the emboli have been 
transported by way of the systemic venous circulation; (2) in other 
parts of the body, when the arterial stream has become infected, either 
from rupture of a purulent focus into it, or from endocarditic thrombi, 
or from metastatic foci in the lungs, or by the passage of small emboli 
through the pulmonary capillaries; and (3) in the liver (suppurative 
pylephlebitis), when the primary focus is in the area of collection of the 
portal vein. 

Terminal or Secondary Infections. — Terminal or secondary 
infections deserve special mention. In the majority of debilitating and 
wasting diseases, such as arteriosclerosis, chronic nephritis, cirrhosis of 
the liver, myocarditis, etc., the final event is determined not by the primary 
disease, but by some secondary or so-called terminal infection. This is 
usually caused by streptococci, staphylococci, or pneumococci, and less 
commonly by Bacillus coli, Bacillus tuberculosis, Bacillus pyocyaneus, 
Bacillus proteus, etc. ; and the infection may be local or general. The 
local infections are the more common, especially pyococcic or tuber- 



PYOGENIC INFECTIONS 65 

culous infection of the serous membranes— pleura, peritoneum, and 
pericardium. 

In the milder pyogenic infections (pyococcic toxemia, sapremia) the 
lesions consist of — usually a local focus of suppuration, cloudy swelling 
of the organs, especially the liver, kidneys, and heart, enlargement and 
softening of the spleen, lessened coagulability of the blood, and often 
small hemorrhages in the serous membranes (pleura, peritoneum, and 
pericardium). In more severe cases, associated with bacteremia (septi- 
cemia), the foregoing lesions are aggravated: to the cloudy swelling of 
the organs foci of necrosis are added, the general lymphatics are enlarged 
and softened, and small hemorrhages appear not only in the serous 
membranes (including the pia-arachnoid), but also in the mucous mem- 
branes and the skin. In the cases usually described as pyemia, in addi- 
tion to the foregoing, thromboses, especially in the region of the primary 
focus, and embolism with infarction and metastatic abscesses in different 
parts of the body, are found. Lesions of the endocardium (acute benign 
and malignant endocarditis) are common in all forms of pyogenic infec- 
tions, and although they often materially modify the course and the symp- 
tomatology of the disease, they scarcely merit separate classification; in 
fact, the nature of the disease is better understood by bearing in mind 
that the involvement of the endocardium is a more or less accidental 
factor in the pyogenic infection, and that although the lesion may be 
serious the essential factor is the general pyogenic infection, of which 
the endocardial lesion may be the least important. The infective bacteria 
may be recovered (in pure X)r mixed culture) from the local lesions and 
the blood. 

Symptoms. — The symptoms vary with the severity of the infection. 
Frequently the onset of the symptoms is insidious, and in case a primary 
local focus (furuncle, wound, puerperium, etc.) is present, a period of 
incubation, varying from one to three or four days, may be quite obvious. 
Occasionally the onset is sudden, with chill or chilliness, fever, malaise, 
headache, general neuromuscular pains and aching, and sometimes 
vomiting and diarrhoea. Especially characteristic is intermittent fever, 
with notable diurnal fluctuations (4° to 6° F.), accompanied by irregularly 
occurring chills and sweats (often the chief complaint). Sometimes the 
fever occurs in paroxysms of hyperpyrexia, between which the tempera- 
ture may be of the continuous-fever type, or almost if not quite normal 
(apyrexia). In addition, the pulse is rapid and weak, the spleen is 
enlarged, diarrhcea may continue, and the headache gives way to restless- 
ness, hebetude, stupor, and delirium; the patient becomes markedly 
prostrated, polynuclear leukocytosis is present, and a high-grade anemia 
develops rapidly. A subicteric hue or even jaundice is not uncom- 
mon, and certain cutaneous phenomena, such as roseola, erythema, 
urticaria, etc., doubtless toxic in nature, may be observed. 

In the so-called pyemic cases, embolic phenomena (mechanical and 
septic infarctions) may occur in all parts of the body, especially: In 
the skin — petechial hemorrhages and furuncles; in the heart — ulcerative 
5 



66 BACTERIAL INFECTIONS 

endocarditis, septic myocarditis, and fibrinopurulent pericarditis; in 
the lungs — hemorrhagic infarcts (pain, dyspnoea, cyanosis, hemoptysis, 
localized dulness, bronchial breathing, and fine rales), abscesses, or 
fibrinopurulent pleuritis ; in the kidneys — renal pain, albumin, blood, and 
tube casts in the urine ; in the spleen — splenic pain, audible and palpable 
frictions; in the eye — retinal hemorrhages, choroiditis, optic neuritis, 
panophthaln#tis ; in the brain — hemorrhage (hemiplegia, monoplegia, 
aphasia, blindness, convulsions) or abscess; in the long bones — 
periostitis and osteomyelitis (local pain and tenderness); in the joints 
— arthritis (local pain, swelling, and tenderness). 

The course of these infections is sometimes extremely rapid, especially 
when a large amount of toxin is suddenly thrown into the circulation; 
death may result within twenty-four or forty-eight hours. Com- 
monly the symptoms last for from one to three weeks; occasionally 
several months. 

Diagnosis. — A primary focus of infection, irregularly occurring fever, 
chills, and sweats, prostration, leukocytosis, anemia, cutaneous hemor- 
rhages and other embolic phenomena, render the diagnosis easy in the 
majority of cases. Confirmation may be obtained by cultivating the 
infective microorganisms from the blood. Involvement of the endo- 
cardium (malignant endocarditis) is suggested by embolic phenomena 
and instability of the cardiac activity (rapid changes in frequency of 
beat). Malaria may be excluded by the presence of leukocytosis, the 
irregularity of the rigors and sweats, absence of the plasmodium, and the 
non-response to quinine. In acute tuberculosis, as contrasted with 
pyogenic infection, variations in the temperature and pulse-rate and 
excessive perspirations occur with more regularity, wasting is more rapid, 
a local focus of tuberculous disease may be detected in some part of the 
body — in the lungs (tubercle bacilli in the sputum), in the pleura, in the 
abdomen, in the brain (tubercle bacilli in the cerebrospinal fluid obtained 
by lumbar puncture) — and embolism does not occur. The detecting of 
chloroidal tubercles in the one case, and of retinal hemorrhages in the 
other, is of the greatest diagnostic value. In case of doubt as regards 
typhoid fever, persistent headache, persistent but not intermittent fever, 
comparative infrequency of the pulse, roseola, tympanites, the Gruber- 
Widal reaction, the recovery of typhoid bacilli from the urine, feces, 
roseola, blood, etc., and the absence of petechia? and of embolism, 
suggest typhoid fever, whereas pyogenic infection is suggested by a local 
source of infection, undue dyspnoea, irregular and repeated rigors, pro- 
fuse sweats, early marked prostration, the rapid development of anemia, 
leukocytosis, embolism, and the recovery from the blood of pyogenic 
microorganisms. In obscure cases of evident intoxication, hidden or 
latent foci of infection, such as gonorrhoea, prostatic abscess, pyelitis, 
osteomyelitis, cholecystitis, etc., should be diligently searched for. We 
are not yet able to distinguish clinically between the different pyogenic 
infections, but in general the streptococcic infections are the more serious, 



ERYSIPELAS 67 

give rise to a more rapid and progressive anemia, greater prostration, 
and often an unusual mental alertness. 

Prognosis. — The outlook depends upon the severity of the infection, 
the resistance of the patient, and the possibility of removing the infectious 
foci. Remarkable improvement often ensues immediately after the local 
foci are removed; if, however, the patient's tissues are already seriously 
damaged, this may avail little, if anything. 

Treatment. — The prime indication is to remove the infectious foci — 
whence the treatment is largely surgical. Little can be expected of 
medicinal measures if the remnants of a putrid placenta are allowed to 
remain in the uterus, or if a liver abscess, brain abscess, or an empyema 
is permitted to go undrained. In addition to surgical measures, the 
patient's strength must be conserved, by fresh air, sunshine, and good 
nutritious food. Whiskey, quinine, iron (tincture of the chloride), and 
strychnine are useful adjuvants — supportive and restorative, and hot 
saline solutions (hypodermoclysis and enteroclysis) assist in eliminating 
the toxins. The coal-tar antipyretics should never be employed. The 
sweats may be controlled by alcohol baths, atropine, and aromatic sul- 
phuric acid. Crede's colloid silver (1 per cent, solution, hypodermically 
and intravenously) has been suggested, but the results have not been 
very encouraging. Antistreptococcic serum has not proved of great 
service. The best results recently have followed the use of autogenous 
vaccines (bacterins); that is, isolating from a local lesion or the patient's 
blood the infecting microorganism and from this preparing a vaccine. 



ERYSIPELAS. 

(St. Anthony's Fire.) 

Erysipelas is an acute, perhaps specific, infectious, and moderately 
contagious disease caused by Streptococcus erysipelatus (Fehleisen), 
and characterized by high fever, marked toxemia, and inflammation 
of the skin and subcutaneous and the mucous and submucous tissues. 
The disease in reality is merely one manifestation of pyococcic infection. 

Etiology. — Erysipelas occurs at all ages, being common in early life, 
in adolescence, and in adult life; but it is rather uncommon in old age. 
It affects males more frequently than females. It is endemic in most 
large cities, and frequently prevails epidemically, especially during the 
late winter and spring; but sporadic cases are common. Recurrences 
are rather frequent; indeed, in some persons one attack seems to 
predispose to subsequent attacks. 

The exciting cause of the disease is Streptococcus erysipelatus, which, 
however, is now believed to be identical with Streptococcus pyogenes. 
Infection may be transmitted by direct inoculation, contact, or proximity 
(possibly transmitted by the air), by a third person, and by fomites — 
whence the frequent occurrence of epidemics (less common recently 
than in former years) in insanitary hospitals, institutions, barracks, etc. 



68 BACTERIAL INFECTIONS 

Susceptibility to the disease is much enhanced by a wound of the skin or 
of a mucous membrane — whence the frequent occurrence of the disease 
(traumatic erysipelas) after parturition, operations, traumatic wounds, 
etc. In many of the so-called idiopathic cases a history of previous 
nasal catarrh may be elicited, and in many others there are doubtless 
unsuspected wounds or abrasions of the nasal or oral mucous mem- 
brane — whence the frequent occurrence of facial erysipelas. Debili- 
tating influences, such as those connected with chronic alcoholism, 
chronic nephritis, cirrhosis of the liver, etc., also favor the development 
of the disease. Infection apparently is usually acquired directly into the 
blood or the lymph channels. 

Pathology. — The lesions consist of the ordinary changes of inflamma- 
tion with marked oedema and cellular infiltration. The streptococci are 
found especially in the lymphatic channels (lymphangitis), and in large 
numbers in the zone of spreading inflammation and beyond (where active 
phagocytosis may be observed). The visceral lesions are those common 
to severe pyococcic infections. Suppuration of the serous membranes is 
rather common — pleuritis, pericarditis,. endocarditis, meningitis, arthritis, 
etc. 

Symptoms. — In so-called idiopathic (non-surgical) erysipelas, the 
period of incubation varies from three to seven or ten days. Often 
prodromal symptoms are absent, but usually there is headache, malaise, 
restlessness, general aching, and loss of appetite ; possibly also slight eleva- 
tion of the temperature. The onset is usually abrupt with a chill or chilli- 
ness (which may be repeated), high fever (104° to 105° F.), sometimes 
nausea and vomiting, followed soon by the specific cutaneous manifesta- 
tions. These develop first on the bridge of the nose or on one cheek 
near the nose, or at a mucocutaneous junction (in the event of a wound, 
however, immediately about the wound). They consist at first of slight 
redness ; at the end of twenty-four hours, however, the skin has become 
red and hot, smooth and glistening, swollen and quite tense (inflammatory 
oedema). The lesions spread by peripheral extension, and are usually 
sharply demarcated from the adjacent unaffected skin by a well-defined, 
elevated, rather pale, and indurated ridge. Often the cheeks, the eyelids, 
the forehead, the ears, sometimes the entire scalp and even the neck 
become involved, and give rise to extreme disfiguration. As the disease 
spreads, the swelling and redness of the parts first affected gradually 
subside. Blebs not infrequently form, especially on the eyelids, fore- 
head, and ears. The cervical lymph nodes are generally much enlarged. 

The systemic disturbance varies much in different cases; it is often 
remarkably slight, as contrasted with the rather severe cutaneous mani- 
festations, but it may be extreme. Usually the fever remains high, with 
slight remissions, for four or five days, and then falls by a rather rapid 
lysis (sometimes even a crisis). The pulse is rapid; albumin is frequently 
present in the urine; and there is often stupor and a moderate amount of 
delirium. . Leukocytosis is present. In favorable cases the subsidence 
of the cutaneous lesions is followed by desquamation (the scales being 



ERYSIPELAS 69 

infectious), and the patient enters upon convalescence. In unfavorable 
cases, the fever remains high, the typhoid state develops, the delirium 
becomes more marked, the urine lessened in amount, the albuminuria 
more marked, and in convulsions or coma the patient may die. In severe 
cases that do not go on immediately to death, more or less extensive 
suppurative (phlegmonous) inflammation, and in some cases, even gan- 
grene, supervenes. Small abscesses are quite common in many otherwise 
mild cases. 

An unusual form of erysipelas has been described — in which the 
cutaneous lesions spread from the face to the neck, to the chest, and 
may even gradually involve the entire body — erysipelas migrans. 
Occasionally the lesions involve the mucous membrane of the nose and 
mouth (usually secondarily, but sometimes primarily), and occasion an 
erysipelatous faucitis which may go on to the most extensive phlegmon- 
ous inflammation and lead to oedema of the glottis, otitis media, inflam- 
mation of the eye and the other orbital tissues, etc. More or less swelling 
and redness of the fauces, however, is not uncommon in cases of ordinary 
erysipelas, and oedema of the glottis may result from extension of inflam- 
mation from without (from the neck). 

Complications. — Pneumonia, pleuritis, pericarditis, malignant endo- 
carditis, meningitis (rarely, however, from extension through the skull, 
as erroneously believed), arthritis, nephritis, and metastatic abscesses 
are the more common complications. 

Diagnosis. — As a rule, the disease is readily recognized. Erythema, 
urticaria, and acute eczema should be distinguished. Erysipeloid of 
Rosenbach (erythema migrans) occurs especially in those who handle 
meat, crabs, and other shellfish, and occasionally in laboratory workers; 
it is characterized by an area of inflammation, usually on the hands, 
sharply outlined, dark, reddish purple in color; and it usually subsides 
within ten days or two weeks. 

Prognosis. — The disease lasts usually ten to fourteen days. The mor- 
tality varies from 4 to 7 per cent. The prognosis is bad in newborn 
infants, in whom the region about the umbilicus is often involved, in 
unusually severe infections, and in aged, debilitated, and alcoholic 
subjects. Recurrences which are not uncommon are frequently due to 
unsuspected erosions of the nasal mucous membrane. 

Treatment. — The regulations enforced in infectious diseases (page 29) 
should be carried out. The patient should be confined to bed, and given 
a light, nutritious diet. Since the disease usually pursues a self-limited 
course, it is doubtful if medicines exert any specific influence; but I am 
in the habit of giving quinine and iron, which are sanctioned by age 
and long experience, and seem to do good : 

3$ — Quinine sulphate 48 grains 30 

Tincture of iron chloride 6 drams 22 j 5 

Glycerin 4 drams 15 

Distilled water, sufficient to make .... 6 ounces 200 — M. 

S. — Two teaspoonfuls (10 c.c). in water, four times a day. 



70 BACTERIAL INFECTIONS 

In mild cases stimulants are not required, but alcohol and strychnine 
should always be given in severe infections, in the aged, and in the 
debilitated. Da Costa obtained good results with pilocarpine subcu- 
taneously, ^ grain (0.01 gram) every two or three hours for three or four 
doses, in the early stages; but assuredly it should be given only to 
sthenic subjects, and never when the disease is advanced. The coal-tar 
products are absolutely contra-indicated. Antistreptococcic serum has 
not yet sustained the claims originally made for it. Better results are 
to be expected from the use of autogenous vaccines (bacterins). 

Locally a saturated aqueous solution of magnesium sulphate, applied 
on a gauze mask, and renewed twice in the twenty-four hours, is the 
best form of treatment; but one may use also applications of cold water, 
lead water and laudanum, mercuric bichloride (1 to 4000), carbolized 
vaseline, or ichthyol ointment (33 per cent.). The injection of carbolic 
acid (2 per cent.), mercuric bichloride, or mercuric biniodide into the 
area of advancing oedema has been practised with some good results 
and many failures; this is also true of painting the area with silver 
nitrate. Judd extols the value of painting the inflamed area and one- 
half inch of the surrounding apparently healthy skin with 95 per cent, 
carbolic acid, and after the painted region has become white applying 
pure alcohol until it becomes pink. Should suppuration ensue, the pus 
should be evacuated surgically. 

For the nervousness, headache, and insomnia, one may use the 
bromides, chloral, opium, and hyoscine. Large amounts of water 
should always be given (as in every toxic process) to facilitate elimina- 
tion of the toxins. The fever, if high, calls for hydropathic measures 
— upon general principles. 



PNEUMOCOCCIC INFECTIONS. 

By pneumococcic infection is understood an infection of the body by 
the pneumococcus, a microorganism first discovered by Sternberg, in 
1880, later studied by Fraenkel and Weichselbaum, and sometimes de- 
scribed as Diplococcus pneumoniae, or Micrococcus lanceolatus. The 
most common manifestation of such infection is the ordinary croupous 
or lobar pneumonia, of genuine cases of which the pneumococcus 
is probably the sole etiological factor. The pneumococcus, however, 
is causative of many other diseases, such as bronchopneumonia, pleuritis, 
pericarditis, endocarditis, peritonitis, meningitis, arthritis, otitis, etc. 
Although these are sometimes primary, they are commonly secondary 
infections, and they may be the result of mixed infections. A number 
of terminal infections in other diseases also are due to the pneumococcus. 
Furthermore, a distinct pneumococcic infection without local lesions, 
a pneumococcic septicemia (bacteremia), may occur. This, which is 
somewhat comparable to typhoid septicemia, typhoid fever without 
intestinal lesions, is usually sudden in onset with chill and fever, but 



PNEUMOCOCCIC INFECTION OF THE LUNG; PNEUMONIA 71 

with few if any local symptoms, and it progresses rapidly to a fatal 
termination under manifestations of profound intoxication — coma and 
collapse of the circulation. The pneumococcus may be cultivated from 
the blood and other tissues of the body. 



PNEUMOCOCCIC INFECTION OF THE LUNG; PNEUMONIA. 

(Pneumonitis; Croupous, Fibrinous, or Lobar Pneumonia; Lung Fever.) 

Pneumonia is an acute, specific, infectious, and mildly contagious dis- 
ease caused by Diplococcus pneumoniae (Sternberg, Fraenkel-Weichsel- 
baum); it is characterized anatomically by bacteremia and a local 
inflammation in the lung proceeding to solidification, and clinically by 
initial chill, rusty expectoration, and high fever that usually ends by 
crisis. 

Etiology.— Pneumonia occurs at all ages, being common prior to the 
sixth year and in adult life and old age. It is less frequent during ado- 
lescence than at any other period of life. It affects males more than 
females, and the urban more than the rural population; and, while it 
frequently attacks those apparently in robust health, it is especially 
prone to attack those debilitated by fatigue, starvation, unhygienic 
surroundings, exposure to the inclemencies of the weather, and over- 
indulgence in alcohol, and those subject to or convalescent from certain 
diseases, such as, influenza, typhoid fever, Bright's disease, diabetes, 
etc. It sometimes follows traumatism to the chest (traumatic pneu- 
monia), and it frequently follows "catching cold" — although this is 
now thought to act merely by reducing the resistance of the individual. 
Recurrences are common, one attack seemingly predisposing to others. 
It is especially fatal in the negro. 

Pneumonia prevails in all parts of the world, and may be said to be 
endemic in most large cities. It is especially prevalent during the 
winter and spring, more particularly in February and March, when 
marked and sudden variations in temperature and humidity are common. 
Small epidemics, especially house (jail, barrack, ship, etc.) epidemics 
are not infrequent. 

The exciting cause of the disease is the pneumococcus, which may be 
found in the lesions in the lung, in the secretions of the entire respiratory 
tract (sputum), in the blood, and sometimes in the complicating lesions. 
It has been found also in the mouths of healthy persons, as well as in 
the dust and hangings of rooms. Pneumonia is slightly contagious — 
some outbreaks more so than others. Infection is usually transmitted 
directly, by a third person, or by the air, although it may be transmitted 
by fomites; it is usually acquired by inhalation, the lung being first 
affected. There is some evidence, however, that the blood may be 
primarily infected, through a wound or the tonsil, for instance, and 
the lung, or other organ, secondarily. Secondary infections with the 
ordinary pyogenic microorganism are not uncommon. 



72 BACTERIAL INFECTIONS 

The pneumococcic process may also be set up by other microorganisms, 
such as Friedlander's pneumobacillus, the influenza bacillus, the typhoid 
bacillus, the plague bacillus, streptococci, staphylococci, etc., but the 
processes induced by these microorganisms differ somewhat anatomically, 
as well as clinically, from true pneumococcic infection of the lung. 

Pathology. — The pneumonic process involves the right lung more 
frequently than the left, because the right bronchus is larger and more 
in a straight line with the trachea than the left, and the lower lobe more 
frequently than the upper. Involvement of the upper lobe in adults 
is often more serious and more likely to terminate fatally than involve- 
ment of the lower lobe; but the upper lobe is often involved in children 
and usually ends favorably. In some cases both lungs are involved, 
whereas in other cases first one portion and then another portion of the 
lung becomes involved. 

Four stages of the process may be described: (1) Congestion; (2) 
red hepatization; (3) gray hepatization; and (4) resolution. Fre- 
quently, however, the lung reveals several stages side by side. In 
the first stage, or stage of congestion, the lung is markedly congested, 
dark red in color, and of increased consistence, although it still crepi- 
tates and floats on water. The capillary bloodvessels are much con- 
gested and dilated — protruding into the alveolar air spaces, which 
are much encroached upon, and which, together with the infundibula 
and the commencements of the bronchi, are more or less filled with a 
tenacious exudate containing erythrocytes, a few leukocytes, and desqua- 
mated alveolar epithelium. As the disease progresses, the exudation in- 
creases until it entirely displaces the air in the alveoli — the second stage 
or stage of red hepatization. Not only the fluid, but also the cellular 
exudate, consisting of erythrocytes, mononuclear and polynuclear leuko- 
cytes, desquamated epithelium, and pneumococci, is increased in amount, 
and the entire exudate becomes coagulated to form a fibrinous mass — 
whence the term fibrinous or croupous pneumonia. The interstitial 
tissues of the lung also show inflammatory phenomena. In this stage 
the affected portion of the lung is increased in consistency, weight, and 
volume (often revealing indentations from the ribs); it is dark, reddish 
brown in color (although less congested than in the first stage); it no 
longer crepitates, and it sinks in water — in a word, it much resembles 
liver tissue, whence the term hepatization. The section surface is con- 
gested (mottled), dry, dull, granular (due to the fibrinous plugs in the 
alveoli), and the organ is quite friable. Red hepatization gradually 
merges into gray hepatization — evidence of increased leukocytic infil- 
tration, lessening of the congestion from pressure upon the bloodvessels 
by the exudation, and beginning autolysis of the exudate. The lung 
becomes mottled, grayish red in color, its surface less granular and 
more moist than previously — the result of degeneration and necrosis of 
the exudate and of the transudation of serum from the bloodvessels. 
The exudate consists in large part of polynuclear leukocytes (phago- 
cytes), although degenerated erythrocytes and desquamated epithelium 






PNEUMOCOCCIC INFECTION OF THE LUNG; PNEUMONIA 73 

may be distinguishable. As the exudate becomes softened, in conse- 
quence of autolytic processes, it is removed, in large part by absorption, 
in small part by expectoration; resolution occurs, and gradually the 
lung returns to its normal condition. In less favorable cases the lung 
may become the seat of purulent infiltration — diffusely infiltrated with 
polynuclear leukocytes and appearing yellowish, soft, and puriform 
to the naked eye. In other cases the lung process goes on to abscess 
formation (one large abscess or several small abscesses that usually 
fuse to form a large one) — due often to secondary infection with 
streptococci and other pyogenic microorganisms; or a portion, or an 
entire lobe, becomesg angrenous — due to defective blood supply and to 
secondary infection with putrefactive bacteria. In other cases resolution 
is delayed and may be followed by induration of the lung or tuberculosis. 

The non-solidified portion of the lung may be normal, but it usually 
shows more or less congestion and oedema. Sometimes there is an 
associated bronchitis, and the fibrinous plugs may extend far into the 
bronchi, forming veritable casts. The pleura investing the affected 
portion of the lung is almost always more or less inflamed, revealing 
usually a fibrinous exudate, although the lesions may progress to serous- 
fibrinous exudation (pleuropneumonia; metapneumonic pleuritis), or to 
suppuration (metapneumonic empyema). The organs in general show 
the results of toxemia and infection. Thus, the bronchial lymph nodes 
are swollen and soft, the myocardium, kidneys, and liver the seat of 
parenchymatous and sometimes fatty degeneration, and the spleen is 
swollen. The heart is frequently markedly dilated (especially the right 
side), and it. may contain firm coagula (attributable to increased fibrin 
in the blood), which may lead to sudden death. Complications such 
as pericarditis, endocarditis, meningitis, enteritis, and other evidences 
of infection are not infrequent. 

Symptoms. — The period of incubation is not definitely known, although 
it probably varies from a few hours to several days. Usually there are 
no prodromal symptoms, but in some cases the patient may complain 
for a day or two of slight catarrh of the upper respiratory tract, malaise, 
loss of appetite, headache, and dull pains in the limbs. In the majority 
of the cases, however, the onset of the disease is sudden — usually with 
a severe chill, but sometimes in children, with a convulsion or vomiting. 
Concurrent with the chill the temperature rises rapidly and attains its 
maximum, 104° F. or more, within a few hours. At the same time the 
patient complains of headache and general muscular or neuromuscular 
pains, severe stabbing pain in the side, cough, rusty expectoration, 
dyspnoea, and the usual concomitants of fever, such as rapid pulse, 
dry skin, a flushed face, loss of appetite, concentration of the urine, etc. 
Soon the physical signs of solidification of the lung and the general 
evidences of toxemia with delirium become apparent. The clinical mani- 
festations continue usually unabated for from five to nine days, in the 
majority of cases, when the crisis occurs, and the patient enters upon 
what is usually a rapid convalescence. 






74 



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PNEUMOCOCCIC INFECTION OF THE LUNG; PNEUMONIA 75 

The Fever. — The fever of pneumococcic infection of the lung is 
quite characteristic (Fig. 2). As already stated, it rises rapidly and 
may reach 104° F. or more, within a few hours. In most, especially 
asthenic, cases the temperature is usually stable, that is, for several days 
the diurnal variations may be not more than a degree. By the third day, 
however, there may be a slight remission and the subsequent diurnal 
variations may amount to 1.5° F., but the temperature remains high until 
some time between the fifth and ninth days (usually the fifth, seventh, 
or ninth, rarely the third, day) when the characteristic crisis occurs — a 
sudden fall of the temperature, within two to ten hours, to normal or less, 
accompanied by profuse sweating, lessening of the dyspnoea and the 
general toxic manifestations, increase in the strength of the pulse and 
the amount of urine, and marked improvement in the general condition 
of the patient, without however, in many cases, any noteworthy changes 
in the physical condition of the lung. Frequently the crisis is followed 
by a prolonged and refreshing sleep. Occasionally the crisis is unduly 
protracted — beyond twenty-four hours. Not infrequently on the day or 
the second day preceding the crisis the temperature falls to between 99° 
and 101.5° F. and rises again — a pseudocrisis. On the other hand, in 
cases with prodromal symptoms and sometimes in children the onset 
may be gradual, and in debilitated and alcoholic subjects the temperature 
range is likely to be relatively low — 102° to 102.5° F. In cases protracted 
beyond the tenth day the fall of temperature is frequently by lysis. In 
some cases the temperature rises before the crisis — a so-called precritical 
rise. Such rise, however, may be merely a forerunner of death, but in 
most cases the temperature falls just before death. Aside from the pre- 
critical hyperpyrexia, the temperature may be unusually high throughout 
the course of the disease — 106° to 107° F. (usually fatal cases); in other 
cases there is no elevation of the temperature whatever — afebrile pneu- 
monia. 

Respiratory Symptoms. — Dyspncea is a constant and characteristic 
symptom, the respirations varying from 30 or more per minute on the 
first day, to 50 or 60 per minute on the third or fourth day; sometimes 
however, reaching 80 to 100 per minute in children. The breathing 
is superficial, repressed, and evidently painful; and the expiration is 
usually accompanied by an almost pathognomonic grunt. The dyspncea 
is not entirely dependent upon the solidification of the lung, being due also 
to pain, fever, toxemia, and loss of functionating lung surface; it is 
frequently out of proportion to the extent of the lung involvement and 
it disappears with the occurrence of the crisis, although the physical 
condition of the lung may persist unchanged for several days. The pulse- 
respiration ratio may become 2 to 1, even 1.5 to 1, instead of the normal 
4 to 1. Pain is an early and distressing sign, and is usually attributable 
to associated involvement of the pleura. It is severe, stabbing in 
character, and much increased by deep inspiration and by coughing. 
It is generally referred to the region of the nipple or the lower ribs on the 
affected side, rarely to the opposite side, or to the abdomen, back, or 



76 BACTERIAL INFECTIONS 

shoulder. It gradually disappears after the third or fourth day. It may 
be slight or absent in central and in apical pneumonias. Cough and ex- 
pectoration are initial symptoms. In the early stages the cough is short, 
harsh, and restrained on account of the pain that it provokes. The 
expectoration, which may be mucous in character for a few hours, speedily 
takes on almost pathognomonic characteristics, becoming rusty, viscid, 
and tenacious. Rarely there is a distinct hemoptysis. In certain asthenic 
cases, the sputum may be thin, less viscid, and darker (more hemorrhagic) 
in color (prune-juice sputum). After the crisis the cough usually becomes 
less harsh and the sputum less viscid and more mucopurulent in char- 
acter. Cough and expectoration may be almost, if not entirely, absent 
in certain asthenic cases, in much debilitated and alcoholic subjects, 
and in the very young and the very aged. Microscopic examination of 
the sputum reveals Diplococcus pneumoniae (often in pure culture, though 
frequently associated with other microorganisms), erythrocytes, leuko- 
cytes, mucus, alveolar epithelium, and sometimes fibrinous plugs from 
the alveoli and casts of the finer bronchioles. 

Circulatory Symptoms. — In ordinary cases the pulse is usually 100 
to 110 or 120, in children 140 to 160, per minute, and full and bounding 
in the height of the disease. Late in the disease, especially if the attack 
be severe, the pulse loses its strength and becomes more rapid (160 or 
more per minute). A pulse of more than 120 per minute, as well as 
a small, weak, and irregular pulse, always occasions concern. In ordinary 
cases the heart sounds are clear and the pulmonary second sound accen- 
tuated. In the height of the disease functional murmurs are common; 
with dilatation of the heart due to weakness of the myocardium, the 
result of toxic degeneration and excessive pressure in the pulmonary 
circulation, relative insufficiency of the mitral and tricuspid valves may 
develop. Early evidence of cardiac embarrassment is furnished by lack 
of muscular tone of the first sound of the heart and weakening of the 
previously accentuated pulmonary second sound; later, there may be an 
extension of the cardiac dulness to the right, epigastric pulsation, and 
embryocardia. Sudden collapse of the circulation — weakness and irregu- 
larity of the heart and the pulse, low blood pressure, subnormal tempera- 
ture, cyanosis, and sweating, are by no means unknown, and are the 
result of toxic paralysis of the vasomotor centres, toxic degeneration of 
the myocardium, and excessive pressure in the pulmonary circulation. 
Though it may prove fatal, it may be recovered from. 

Blood. — Polynuclear leukocytosis is a diagnostic feature of most cases. 
The leukocytes usually number from 18,000 to 45,000 per c.mm.; 
they may be more numerous (rare), and in extremely asthenic and 
toxic cases there may be little or no leukocytosis (a bad prognostic 
sign). Leukocytosis begins with the onset of the disease, persists through- 
out its course, and falls with and after the true crisis. During the 
height of the disease the eosinophiles are much reduced or absent; 
they reappear with or just prior to the crisis. The other blood changes 
consist of a secondary oligocythemia and oligochromemia, rapid clotting 



PNEUMOCOCCIC INFECTION OF THE LUNG; PNEUMONIA 77 

of the blood, due to increase of the fibrin elements, and the presence of 
the diplococcus in some cases. 

Nervous Symptoms. — Nervous symptoms are a characteristic of 
all cases. Headache, mental dulness, and at least slight mental wander- 
ing, are rarely missed. In well-developed cases, delirium is constant, 
although it varies in character. It may be maniacal, but it is usually 
of a low adynamic muttering character (profound toxemia), or it may 
resemble delirium tremens (true delirium tremens is the rule in alcoholic 
subjects). Convulsions are common at the onset in children, and some 
cases of pneumonia in children run their course altogether under the 
guise of meningitis (so-called cerebral pneumonia). Cerebral symptoms 
sometimes develop about the time of, or persist after, the crisis, and, con- 
sisting of mental hebetude, delirium, rarely of insanity, they may continue 
for several days. 

Digestive Symptoms. — Initial vomiting is common, especially in 
children. The tongue is coated with a white or yellowish white fur and 
later sordes not infrequently collect upon the teeth and gums, and the 
tongue may become fissured. Thirst is marked, the appetite is lost, 
and the patient is usually constipated, unless enteritis or colitis develops. 
Meteorism, sometimes of dangerous grade, since it embarrasses the 
already embarrassed heart and lungs, may accompany the pneumococcic 
enteritis or colitis, or it may be due to toxic paresis of the intestine. 
The spleen is usually enlarged and palpable, and the liver can often 
be felt, especially in right-sided pneumonias, in which an apparent 
enlargement may be due only to displacement of the liver downward. 

Cutaneous Symptoms. — Herpes occurs in about one-third of the cases 
on the lips and about the alee of the nose, but occasionally also on the 
cheek, ear, arms, genitals, etc. It develops usually on the second, 
third, or fourth day of the disease, and sometimes comes out in successive 
crops. Moderate sweating is common throughout the latter half of the 
disease, and profuse sweating occurs with the crisis. A dusky flush 
on the cheek, said to be homolateral with that of the lung affected, is 
quite common; sometimes the flush occurs on both cheeks, being more 
marked on that of the side affected with pneumonia. 

Urinary Symptoms. — The urine presents the characteristics of febrile 
urine — concentrated, lessened in amount, high colored, increased in 
specific gravity, and depositing a copious sediment of urates and uric 
acid. Albumin, referable to toxic changes in the renal epithelium, is 
common; sometimes a true nephritis (much albumin, blood, and tube 
casts) develops. The chlorides are usually much diminished, or absent 
throughout the height of the disease. The diazo reaction is sometimes 
present. 

Physical Signs. — In the first stage, or stage of congestion (usually 
of not more than twenty-four hours' duration), the respiratory move- 
ments over the affected portion of the lung are restricted; there is slight 
increase of tactile fremitus and of vocal resonance; the percussion note 
may be normal, but is usually higher pitched and somewhat tympanitic 



78 BACTERIAL INFECTIONS 

(Skodaic resonance) ; and the breath sounds are weak or bronchovesicular 
in character. The crepitant rale of Laennec may be heard. This is 
usually said to be due to forcible separation of the alveolar walls and 
infundibula rendered adherent by the viscid exudation; in some cases, 
however, a sound indistinguishable therefrom is more likely a pleural 
friction, since it is not heard in all cases, and not until the end of the 
first stage, when the pleura may be covered with a layer of fibrin. 

In the second stage, or stage of solidification, the respiratory move- 
ments over the affected portion of the lung are much restricted, while 
those over the other lung are exaggerated; the affected side may be 
somewhat enlarged (1 to 1.5 cm.), but the intercostal depressions are not 
obliterated. Tactile fremitus and vocal resonance are much increased, 
except in the exceptional cases in which the bronchi are plugged by 
mucus or fibrinous exudate, or when there is an associated pleuritis. The 
percussion note is dull — there being varying grades of dulness from the 
slight dulness of the first stage to marked dulness or flatness, present 
especially posteriorly, in the fully developed disease. With the dulness 
there is increased resistance to the percussing finger, but neither the 
dulness nor the resistance are as marked as in pleuritis with effusion. 
Dulness is less marked in incomplete solidification, especially in pneu- 
monias that do not fully reach to the surface (central pneumonias), 
in the very young, and in the aged (on account of senile changes in the 
ribs and cartilages). Skodaic resonance may be elicited above the 
solidified area. The breath sounds are bronchial or tubular in character, 
though rarely they may be absent in case the bronchi are plugged with 
exudate; a voluntary cough, however, will usually dislodge such plug, 
which, being followed immediately by bronchial breathing, is conclusive 
evidence of solidification. Bronchophony, sometimes egophony, may 
be elicited (unless the bronchi be plugged). I have known Wintrich's 
change of note and amphoric breathing to lead to confusion with a 
cavity. In associated bronchitis, fine, crackling rales may be heard, 
and usually with undue distinctness on account of the solidification. 
The uninvolved lung reveals exaggerated vesicular breathing, and occa- 
sionally, especially in children and young subjects, bronchial breathing 
due to conduction from the diseased lung. 

With the onset of resolution there is a gradual return to the normal 
conditions. Movement returns to the previously immobile chest, tactile 
fremitus and vocal resonance lessen, and the percussion note becomes 
less dull, more tympanitic, and finally resonant (although more or less 
impairment of the note may persist for a long time). The breath sounds 
become less bronchial, bronchovesicular, and finally (but often not for 
a long time) purely vesicular, and coarse and fine bubbling rales, together 
with in some cases the recurrence of the crepitant rale (so-called redux 
crepitus), make their appearance. In some cases the physical signs are 
much delayed, although the diagnosis is quite evident from the symp- 
toms — chill, fever, pain, cough, rusty expectoration, and dyspnoea. In 



PNEUMOCOCCIC INFECTION OF THE LUNG; PNEUMONIA 79 

some cases physical signs are never found. I have known them to be 
delayed until nearly or about the time of the occurrence of the crisis. 

Clinical Varieties. — A number of terms have been employed to designate 
different varieties of pneumonia. Thus basal pneumonia is sufficiently 
explanatory of the majority of cases. Apical pneumonia is common in 
children, more likely to be attended by cerebral symptoms and profound 
intoxication, and often escapes detection because of the frequent slight 
cough and expectoration, and because the apices posteriorly are not care- 
fully examined. In adults it is said to be more fatal than the basal form. 
Double pneumonia is that form in which both lungs, or portions of both 
lungs, are involved. Migratory, or creeping pneumonia, is that in which 
different portions of one or both lungs are successively involved. In this 
the onset may be gradual, the course is prolonged, exacerbations are 
common, and the disease usually ends by lysis. Massive pneumonia 
is a form in which an entire lung, or at least a large portion of a 
lung, is involved and the fibrinous exudate extends from the alveoli to 
the bronchi. Casts of the bronchi revealing dichotomous divisions may 
appear in the sputum. The physical signs much simulate those of 
pleurisy — there being flatness, absence of breath sounds, and of tactile 
fremitus and vocal resonance. The diagnosis is sometimes suddenly 
cleared up by the expectoration (by voluntary or involuntary coughing) 
of obstructing plugs of exudate, and the immediate development of 
characteristic physical signs. Central pneumonia is that in which the 
process commences in the centre of a lobe, and, spreading gradually 
to the surface, does not immediately occasion demonstrable physical 
signs, and in which the diagnosis, for a time at least, rests upon the symp- 
toms. Latent pneumonia is that which pursues its course unsuspected 
for some time, or altogether. Many cases of central pneumonia are of 
this nature, as is also pneumonia in the aged, and many cases develop- 
ing in the course of Bright's disease, insanity, and alcoholism. In 
alcoholics, especially, pneumonia is frequently entirely unsuspected, 
the symptoms being attributed to meningitis, delirium tremens, or 
uremia. 

Epidemic pneumonia, as the term implies, is an epidemic form of 
the disease. It may be widespread or local. Thus, family, house, jail, 
ship, etc., epidemics are well recognized. These often have a high mor- 
tality rate, and may be associated with influenza. Larval, or abortive, 
pneumonia is a form of short duration and usually mild symptoms, com- 
mon especially during epidemics. The initial chill, fever, cough, rusty 
expectoration, and ill-defined or negative physical signs may be followed 
by complete recovery in a few days. Alcoholic pneumonia, pneu- 
monia in alcoholics, is usually attended by marked nervous symptoms 
and delirium, and is often devoid of suggestive local manifestations. It 
is insidious in onset, has a relatively low fever range (101° to 102° F.), 
and a very high death rate. Typhoid pneumonia is a pneumonia charac- 
terized by marked asthenia or adynamia (asthenic or adynamic pneu- 
monia) or the typhoid state (and has nothing whatever to do with typhoid 



80 BACTERIAL INFECTIONS 

infection or typhoid fever). The characteristic of the disease is extreme 
toxemia (toxic pneumonia) — whence it indicates severity of infection 
and sometimes double infection (pneumococcic and streptococcic or 
staphylococcic, bacteremia being common). It must be distinguished 
from pneumotyphoid — typhoid infection of the lung occurring in the 
course of typhoid fever. It is also true that pneumococcic infection 
of the lung may occur in typhoid fever. Bilious or malarial pneumonia 
is a term used by some writers to designate pneumonia occurring espe- 
cially in malarious regions, and attended by jaundice, vomiting, and 
severe nervous symptoms. The complicating symptoms are usually 
due to an associated duodenal catarrh, and bear no relation to the 
malarial parasite, although infection with the pneumococcus and the 
malarial parasite (as well as with other microorganisms) may be con- 
current. 

Secondary pneumonia is common in many of the acute infective 
diseases. It may be due to the pneumococcus or to the microorgan- 
isms provocative of the primary disorder (typhoid fever, diphtheria, 
etc.), or to mixed infection with streptococci, staphylococci, and colon 
bacilli, etc. It is generally bronchopneumonic in type, and devoid of 
most of the characteristic clinical and anatomical features of true lobar 
pneumonia. Terminal pneumonia (usually bronchopneumonia) is a 
common event in the final stage of many cases of Bright's disease, 
diabetes, carcinoma, heart disease, and the adynamia of senility. The 
onset is gradual and the symptoms slight and not suggestive; there 
may be, indeed, few clinical manifestations aside from dyspnoea and 
slight fever. 

Pneumonia in the aged is often latent, and may be terminal. The 
onset may be sudden, but it is usually insidious, and the local symptoms 
and physical signs are slight, although the patient is manifestly seriously 
ill and usually soon dies from cardiac debility. This is a hypostatic or 
bronchopneumonia, and is especially common in the aged who are con- 
fined to bed — as with a fractured femur, for instance. Pneumonia in 
children and infants often begins with a convulsion or vomiting, the 
apex is often involved, cerebral symptoms are marked (the disorder 
much simulating meningitis), expectoration is absent, and the disease 
usually ends in recovery. 

Postoperative and ether pneumonia occurs sometimes after operation 
and anesthetization, especially after abdominal operations (probably 
because the bronchial secretions are allowed to accumulate on account 
of the pain provoked by coughing). The development of the disease 
is much favored by winter season, by prolonged anesthetization, general 
debility of the patient, disease of the respiratory tract, such as bronchitis 
or chronic congestion from heart disease, and by the aspiration of irrita- 
ting particles (aspiration or inhalation pneumonia). It is often lobular 
(that is, bronchopneumonia) rather than lobar, insidious in onset, latent 
in course, and frequently due to microorganisms other than the pneu- 
mococcus. 



PNEUMOCOCCIC INFECTION OF THE LUNG; PNEUMONIA 81 

Complications and Sequels. — Inflammations of the serous membrane, 
pleuritis, pericarditis, endocarditis, and meningitis, are common com- 
plications — pleuritis the most common, and meningitis the most serious. 
In most of these complicating exudates, the pneumococcus may be 
detected, sometimes alone, sometimes in association with the strepto- 
coccus, staphylococcus, etc. Pleuritis is a part of the pneumonic process 
rather than a complication, since it occurs in all cases in which the inflam- 
mation reaches the surface of the lung. In most cases the exudate is 
slight in amount and fibrinous in character; in other cases it is serofibrin- 
ous, and more or less abundant (pleuropneumonia, metapneumonic 
pleuritis). In still fewer cases, however, but rather commonly in children 
and youths, the exudate is purulent (metapneumonic empyema): most 
cases of supposed, unresolved pneumonia. Unusual prolongation of 
the disease, chills, fever, sweats, leukocytosis, flatness on percussion, 
markedly increased resistance, absence of breath sounds and of rales, 
suggest the presence of the pleural lesions; but an absolute diagnosis 
may require the use of the exploring needle. Pericarditis is a rather 
unusual complication, more common in left-sided than in right-sided 
pneumonias. It is usually fibrinous, but may be serofibrinous or puru- 
lent. Its presence may be inferred from the development of undue dys- 
pnoea and pericardial distress, but its diagnosis depends upon the detection 
of the physical signs. Acute endocarditis, both simple and malignant, is 
more common; it affects the left side of the heart rather than the right, 
especially if there be an old valvular lesion. The diagnosis rests upon 
detecting the ordinary manifestations of acute endocarditis — sepsis 
and embolic phenomena. Acute meningitis, usually fibropurulent, is 
a rather uncommon, and usually fatal, complication. Frequently it 
cannot be distinguished from the meningism of many cases of pneumonia 
without resort to lumbar puncture, which may reveal pneumococci in 
the meningeal exudate. That the pneumococcic process is a more or 
less widespread infection in many cases is evident from the occurrence 
together of inflammation in divers organs, such as the lung, pleura, 
endocardium, meninges, etc. Rarer complications are bronchitis, 
pneumococcic synovitis and arthritis, toxic degeneration of the myo- 
cardium, gastritis, duodenitis (causing jaundice), enteritis, colitis, 
nephritis, peritonitis, neuritis, phlebitis, heart clots, etc. 

Sequels are rare, inasmuch as most cases result in recovery. In some 
cases, however, relapse occurs; that is, a few days after the crisis the 
fever returns and persists for several (two to seven or eight) days. 
Recurrences are common — one attack seemingly predisposing to others, 
and eighth, ninth, and tenth attacks being by no means unknown. In 
some cases resolution is much delayed, and although it may ultimately 
occur after many days or several weeks, the lung being restored to 
the normal, fibroid induration (chronic interstitial pneumonia) is a 
very likely event. In other cases purulent infiltration or abscess (single 
or multiple), gangrene, or tuberculosis results. 
6 



82 BACTERIAL INFECTIONS 

Diagnosis. — In the majority of cases, especially in sthenic subjects, 
the disease is rarely overlooked — the abrupt onset, initial chill, pain in 
the side, dyspnoea, cough, rusty expectoration, herpes, leukocytosis, 
physical signs of solidification of the lung, and the course of the fever, 
being unequivocal. In debilitated subjects, in those the subject of 
chronic disease, and in the aged, the disease setting in insidiously may 
escape recognition. Undue dyspnoea and fever should suggest a physical 
exploration of the lungs. The association of fever and delirium tremens 
should lead to the suspicion of pneumonia in an alcoholic subject. 

The diseases with which pneumonia is most likely to be confounded 
are typhoid fever, pleuritis with effusion, meningitis, bronchopneumonia, 
and acute pneumonic tuberculosis. Cases of acute pneumonic tuber- 
culosis, often said to be the consequence of the engrafting of tuberculosis 
upon a primary pneumococcic infection, are almost always tuberculous 
from the onset. In the majority of cases the tuberculous nature of the 
infection is not recognized until the expected crisis does not occur or 
tubercle bacilli and elastic fibers are detected in the sputum. The tuber- 
culous nature of the disorder, however, may be suggested by previous 
ill health of the patient, tuberculosis in the antecedents, a gradual 
onset, an intermittent and later remittent fever, hemorrhagic-purulent 
and non-viscid sputum, profuse sweats, rapid emaciation, and the physical 
signs of cavity formation. In other cases, a later involvement of one 
apex suggests that the primary lesions (which are more frequent in the 
upper than in the lower lobe) were tuberculous. 

Prognosis. — Pneumonia is a very fatal disease — the mortality rate being 
from 15 to 40 per cent. The prognosis is influenced by: (1) The age 
of the patient. Children usually recover; the aged usually die. The 
mortality rate increases with each decade beyond the second. (2) Race. 
The disease is more fatal in the negro than in the white race. (3) The 
previous health of the patient. The death rate is high in those debili- 
tated from any cause. It is almost always fatal in alcoholic subjects. 
(4) The severity of the infection. The prognosis is bad in patients with 
marked toxemia, persistently high temperature (105° F. and more), 
cardiac weakness, and absence of leukocytosis. The extent of the lung 
involvement, unless it be extreme and bilateral, has very little influence 
on the severity of the symptoms (the degree of toxemia). (5) The pres- 
ence of complications renders the prognosis much more anxious, as almost 
all deaths in previously healthy subjects occur in complicated cases. 
Death in uncomplicated cases is due to the general effects of the toxemia, 
or to the special effects of the toxemia on the heart associated with the em- 
barrassing results of increased intrapulmonary pressure, or to heart clot. 

Treatment. — Although the patient is not notably infectious to those 
about him, it is well that he be isolated; the sputum undoubtedly should 
be destroyed, since it unquestionably is the chief source of infection; 
and it is wise also, especially if several cases of pneumonia have occurred 
in the same room or the same bed to disinfect the bed and the room 
(see page 29). 



PNEUMOCOCCIC INFECTION OF THE LUNG; PNEUMONIA 83 

Our general management of the patient should always be guided by a 
knowledge of the fact that pneumococcic infection of the lung is self- 
limited, and that we are apparently unable to shorten it or to influence the 
crisis. Still we can unquestionably do a great deal for our patients. I 
have not been able to assure myself that the disease can be aborted, even 
in its very earliest stages; from time to time I have used the different 
measures recommended for this purpose, such as venesection, aconite, 
veratrum viride (to bleed the patient within his own vessels), large 
doses of digitalis (with a view forcibly to stimulate the heart and re- 
establish the cardiopulmonary circulation); but,, although the patients 
recovered without untoward symptoms, the disease was not aborted. 
After the disease has become established, that is, after the first twenty- 
four hours, these methods of treatment, except bleeding (to be referred to 
presently), are as harmful as they are irrational. 

The patient should be placed in a large, readily ventilated room, and 
the windows should be kept wide open all the time, so as to provide an 
abundance of fresh air. When available, as in hospital practice, the 
best results are achieved by placing the patient out-of-doors, as on a 
porch, for instance; he should, of course, be well protected by a suffi- 
ciency of bed-clothes. The fresh air tends to promote an efficient aera- 
tion of the blood, it lessens the cyanosis, invigorates the cardiovascular 
system, reduces the general intoxication, etc. There can be no com- 
parison between the results attained by affording the patient from the 
beginning an abundant supply of fresh air, and those that ensue upon 
the giving of canned oxygen when cyanosis has become extreme and 
the patient's vitality has been almost if not quite depleted by the 
intoxication. 

In the early stages of the disease, at least, the diet should be largely 
fluid, that is, largely milk; but the milk may be flavored, as recom- 
mended for the typhoid-fever subject, or it may be given as junket, etc. ; 
and there can be no serious objection to egg-white or the w T hole egg (if 
well borne), or to meat and vegetable soups thickened with a little 
flour, powdered rice, or barley, or strained oatmeal gruel, cornstarch, 
arrow-root, blanc-mange, gelatine flavored with wine, calf's-foot jelly, 
etc. Care must be taken not to overfeed the patient. After the crisis, 
milk toast, scraped meat, soft-boiled eggs, potato puree, stewed fruits, 
etc., may be added, and in a day or two sweetbreads, chicken, etc. 

The special indications for treatment are to combat the toxemia, to 
support the overtaxed heart, to relieve certain symptoms, and to treat 
the complications as they arise. As yet we have no specific. Anti- 
pneumococcic serum has not realized the claims originally made for it; 
nor is this to be expected a priori, since the pneumococcic toxin is an 
intracellular rather than an extracellular toxin — whence the difficulty of 
producing an efficient antitoxin. I have used the serum in a few cases, 
apparently with some influence on the temperature, and a slight, though 
doubtful, influence on the toxemia. Encouraging results have recently 
followed the use of bacterial vaccines and of extracts of washed leuko- 



84 BACTERIAL INFECTIONS 

cytes; but sufficient use has not yet been made of these forms of treat- 
ment to determine finally their value. 

The pain of the early stages is best relieved by twenty to forty dry cups 
placed on one or both sides; these not only relieve the pain, but also 
lessen the dyspnoea. The cupping may be repeated twice or thrice 
within the first twenty-four hours, and again during the second twenty- 
four hours, if required. Should this be ineffectual, morphine should 
be given hypodermicly, since pain itself is depressing to the patient and 
must be relieved. Dover's powder, deodorized tincture of opium, an 
ice-bag, a Leiter's coil, a light application of the Paquelin cautery, or 
strapping the side, also may be used; or one may give every three or four 
hours a pill containing quinine sulphate, 2 grains (0.13 gram), and 
powdered opium, J grain (0.03 gram).' This not only relieves the pain 
and promotes a feeling of general well-being, but is believed to exert 
also some antiphlogistic action. I have long since given up the use of 
poultices, the newer clay poultices as well as the better, though more old- 
fashioned, flaxseed poultices — with considerable increase in the general 
comfort of my patients. A cotton jacket may be applied to a child — 
and will do the mother considerable good. During this stage the blood 
pressure, if high, may be reduced — by bleeding, free catharsis, and 
diaphoresis. The abstraction of twenty ounces of blood in sthenic 
subjects is often followed by relief of pain, dyspnoea, and cerebral 
(toxic) symptoms; but it should not be practised indiscriminately, and 
not in debilitated subjects. An initial dose of 10 grains (0.6 gram) of 
calomel, followed by a saline cathartic, subserves a very useful purpose, 
promoting free evacuation of the bowels and reducing the blood pressure. 
If given dry on the tongue and allowed to mix with the secretions of the 
mouth and throat it exerts also a local antiseptic action. Potassium 
citrate, solution of ammonium acetate, spirit of nitrous ether, etc., also 
promote the comfort of the patient by inducing sweating, reducing the 
blood pressure, and promoting diuresis and elimination of toxins. 

The use of hydrotherapy, of water internally and externally, is the 
best means at our command to combat the effects of the toxemia : given 
internally, being our best diuretic, it promotes the free discharge of toxin 
with the urine ; applied externally, by its stimulating effects, it counteracts 
the depressing effects of the toxins. An excellent procedure is to envelop 
the chest with cloths wrung out of water at a temperature of from 
50° to 32° F., to cover these with several thicknesses of dry flannel, and 
to leave them on for from fifteen to thirty minutes, depending upon the 
reaction. Often the dyspnoea and the cyanosis are relieved, the pulse 
becomes stronger, fuller, and less rapid, the manifestations of cerebral 
intoxication lessen, and the temperature falls to 100° F. or less. The pro- 
cedure may be repeated every two to four hours, should the temperature 
again become high and other, especially nervous, evidences of toxemia 
again become marked. In other cases excellent results follow the appli- 
cation of cloths wrung out of ice water and changed every fifteen minutes 
for two hours ; the treatment may be repeated after an interval of two 



PNEUMOCOCCIC INFECTION OF THE LUNG; PNEUMONIA 85 

hours during the day and of four to six hours at night. The indication 
for repeating the hydrotherapeutic measures is found in the reaction of 
the patient. Cool spongings also are sometimes of service. Full tub 
baths have been recommended, but I have not been convinced of 
their utility. Warm, full baths, however, are often useful in children. 
Although the degree of the temperature is utilized as one of the indica- 
tions for the use of hydrotherapy, the fever, as such, unless very high, 
really does very little harm, and it is not necessary to reduce it at all 
hazards; when very high it may be reduced by hydrotherapeutic 
measures. Under no circumstances whatever should any of the anti- 
pyretic drugs be used; they are a distinct menace to the pneumonic 
patient, reducing his vitality, weakening the heart, lowering the tone 
of the cardiovascular or vasomotor system, and reducing the oxygen- 
ation of his tissues (increasing cyanosis) — only assisting, therefore, the 
pneumococcic toxin to kill the patient. That they are sometimes given 
to patients who recover is but one of the many indications of the wonder- 
ful resisting powers of the human system. 

Whether or not the temperature is high, the patient should be sponged 
two or three times in the twenty-four hours with cool or tepid water — to 
promote cleanliness and a general feeling of well-being, to allay nervous 
irritability and induce sleep ; if the temperature is also somewhat reduced 
this is an additional advantage. 

Water internally is of even greater service, since it promotes the free 
elimination of the toxins. At least three liters should be given to an 
adult within the twenty-four hours. One of the mild alkaline diuretics, 
such as potassium bicarbonate, acetate, or citrate, or lemon juice, lime 
juice, or other fruit juice may be added to it. In the event of renal 
elimination being inadequate and toxemia increasing, hot enteroclysis 
and hvpodermoclysis (sometimes even intravenous injection) of normal 
saline solution should be used systematically and repeatedly. 

Delirium and other nervous manifestations of toxemia call for stimu- 
lants, of which strychnine and alcohol are the best. Strychnine may be 
given routinely to all patients when toxemia is marked, the heart weak, 
and renal elimination low; it is wise to begin it early in the hope of averting 
some of the dangers that threaten. Alcohol had best be withheld until 
it is required — when it will often tide the patient over the critical period 
of his disease. From four to eight ounces of whiskey or brandy daily 
usually suffices. Champagne is excellent for a short time. The more 
diffusible stimulants, such as cocaine, the aromatic spirit, the carbonate, 
and other preparations of ammonium, compound spirit of ether, camphor, 
etc., are useful adjuvants when the heart is failing. Late in the course 
of the disease, when the heart is dilating from increased intrapulmonary 
pressure, I have seen excellent results from the use of tincture of digitalis, 
8 to 10 minims (0.5 to 0.6 c.c), combined with 5 to 8 minims (0.3 to 
0.5 c.c.) of tincture of belladonna (to increase the vascular tone), every 
three or four huurs. Digitalin, -^ grain (0.005 gram) hvpodermicly, 
may be substituted for the tincture of digitalis. Caffeine also is of 



86 BACTERIAL INFECTIONS 

much value. Atropine hypodermicly is of good service when there is 
oedema of the lungs and the vascular tone is low; but when vasomotor 
paralysis supervenes the best results follow the use of hypodermoclysis 
or intravenous transfusion of physiological saline solution with adrenalin 
chloride. Finally, when the cyanosis becomes marked, the heart's action 
feeble and irregular, the muscular element of the first sound of the heart 
indistinct, and the previously accentuated pulmonary second sound weak, 
when, in other words, dilatation is marked, good results attend vene- 
section, which may be followed by hypodermoclysis or intravenous in- 
jection of normal saline solution with adrenalin chloride. Nitroglycerin 
is said to be of value when the blood pressure is high, but this is seldom 
the case. I have never seen much good from its use : indeed, it is usually 
directly contra-indicated. When the toxemia increases to such an extent 
as to simulate meningitis (the meningism of the French) lumbar puncture 
may be practised with hope of good results. 

A sufficiency of sleep should be assured the patient — by the mentioned 
hydrotherapeutic measures, a Dover's powder at night, hot whiskey, a 
small dose of morphine, or one of the hypnotics. Cough, as such, 
rarely requires treatment, but in case it is painful and distresses the 
patient it may be controlled by an occasional Dover's powder, codeine, 
or heroin. Expectorants, as a rule, are not indicated, usually not until 
the stage of resolution, when, if the sputum is viscid and tenacious, 
ammonium chloride, iodide, or carbonate, terpene hydrate, terbene, 
and similar drugs may be used. Should tympany develop it must be 
relieved immediately — since it adds to the already existing embar- 
rassment of the heart and lungs; the diet must be regulated, milk 
stopped, the bowels opened freely, eserine, y^- to -^j- grain (0.00065 
to 0.0013 gram) given hypodermicly, and efforts made to increase the 
usually low blood pressure. 

The complications and sequels are to be treated on general principles. 
General tonics, iron, quinine, strychnine, cod-liver oil, phosphorus, 
etc., are valuable during convalescence. In delayed resolution, recourse 
may be had to these general measures, and to counterirritation (iodine, 
blisters, the Paquelin cautery), the iodides internally, and perhaps the 
cautious use of the x-rays, which although not free from danger, are 
said to foster resolution. Pilocarpine has been recommended, but it is 
doubtful if it does any good. 



MENINGOCOCCI INFECTION; CEREBROSPINAL FEVER. 

(Epidemic Cerebrospinal Meningitis; Spotted Fever.) 

Cerebrospinal fever is an acute, specific, infectious, and slightly con- 
tagious disease caused by Diplococcus intracellularis meningitidis (Weich- 
selbaum) ; it is characterized anatomically by fibrinopurulent inflamma- 
tion of the pia-arachnoid, and clinically by irregular course, fever, and 
divers nervous symptoms. 



MENINGOCOCCI INFECTION; CEREBROSPINAL FEVER 87 

Etiology. — Cerebrospinal fever, though it occurs at all ages and in 
both sexes, is more common in children and young adults, and in the male 
sex. It occurs both epidemically and sporadically, especially in the 
winter and spring; epidemics are usually circumscribed, rarely wide- 
spread, are often more common in country villages and towns than in 
larger cities, and are much favored by overcrowding and general insani- 
tary conditions (institutions, barracks, jails, etc.). 

The exciting cause of the disease is Diplococcus intracellularis menin- 
gitidis (or meningococcus), which is found in the cerebrospinal exudate, 
and sometimes in the nasal secretions and the blood. The disease does 
not appear to be especially contagious. How the contagium is spread 
is not definitely known, but acute and chronic meningococcic "carriers" 
seem sometimes to be the active factor. Fomites are not unduly active. 
Infection is believed to be acquired through the nose (infecting the men- 
inges through the cribriform plate of the ethmoid bone or through the 
sphenoidal cells); doubtless the ear is sometimes the portal of entry, 
and possibly the blood is sometimes primarily involved (by way of the 
tonsils, etc.). Recurrences are not uncommon; one attack does not 
confer immunity. 

An infection almost if not quite identical, anatomically and clinically, 
with cerebrospinal fever may be caused by the pneumococcus, strepto- 
coccus, staphylococcus, influenza bacillus, etc., but these are usually 
secondary infections. 

Pathology. — In the early stages there is intense hyperemia of the pia- 
arachnoid; in fulminant cases these may be the only lesions observed. 
In the ordinary acute cases, there is sero-fibrino-purulent inflammation 
of the pia-arachnoid, especially marked at the posterior basic region of the 
brain, and the dorsal surface of the thoracic and lumbar cord ; but the exu- 
date may extend to the convexity of the brain, and indeed involve the entire 
pia-arachnoid. The cranial nerves (especially the second, third, fourth, 
fifth, sixth, seventh, and eighth) are often embedded in a thick, fibrino- 
purulent exudate, whereby irreparable damage results. In more chronic 
cases the pia-arachnoid is irregularly thickened, the ventricles are dis- 
tended with turbid fluid, and irregular foci of hemorrhage, softening, 
and encephalitis are encountered. Microscopically the exudate consists 
largely of polynuclear leukocytes, which contain the meningococcus and 
certain unusually large endothelial cells; there is also leukocytic infiltra- 
tion of the brain and cord, foci of hemorrhage and suppuration, and 
swelling of the ganglion and neuroglia cells. The lesions common to 
most toxemias are found in the other organs. 

Symptoms. — The period of incubation is probably short — one to four 
days. Usually prodromes are slight — malaise, headache, pains in the 
back, etc. ; but they may be entirely absent. The onset of the disease 
is commonly abrupt, with severe chill (sometimes chilliness), fever 
(102° to 103° F.), severe headache, vomiting, soon followed by pain and 
stiffness in the muscles of the neck. Evidences of general involvement 
of the nervous system are soon manifest in increasing headache, vertigo, 



88 BACTERIAL INFECTIONS 

vomiting (sometimes intractable), delirium, which in the early stages 
may be wild and maniacal, but with increasing exudation gives way to 
stupor and finally coma. Involvement of the special senses is seen in 
early photophobia and intolerance of noises, followed by paretic phenom- 
ena — dimness of vision and deafness. Evidences of motor irritability 
are always seen, and consist especially of spasm of the muscles of the 
neck (painful retraction of the head) and of the spine (opisthotonos), 
increased reflexes, tremors and clonic and tonic spasms of other muscles, 
of which Kernig's sign is an important evidence — inability to extend the 
leg when the thigh has been flexed upon the abdomen; this, which may 
be readily accomplished in health, is rendered impossible in most cases 
of meningitis by the tonic spasm of the flexors of the leg (the ham-string 
tendons). The ocular and the facial muscles also may be implicated 
in the spasms. Later, evidences of paresis or paralysis become manifest; 
these, while they may be present in the extremities (monoplegia, para- 
plegia, etc.), are commonly most marked about the eye (ptosis, unequal 
pupils, strabismus, etc.) and the face. Evidences of sensory irritability 
are found in the general cutaneous hyperesthesia, tenderness of the 
skull and along the spine, and sometimes of the peripheral nerves. 
Anesthesia sometimes replaces the hyperesthesia. 

The fever is irregular — remittent and intermittent, sometimes sub- 
normal, sometimes very high (105°, 106°, even 108° F. or more just before 
death). The pulse is variable; it is often accelerated at first, especially 
in children, but in many cases, especially in adults, it soon becomes 
very slow — 60, 40 — and irregular, and it varies much from time to time. 
The respirations are often increased at first; soon they become normal 
(except in the event of pneumonia or bronchitis) ; later they may take on 
the Cheyne-Stokes type. Herpes facialis occurs in about 60 per cent, 
of the cases. Petechia? (whence the name spotted fever) occur in some- 
what more than one-half of the cases in most epidemics; in sporadic 
cases they are often missed; and when present may be few or many 
(universal). Trousseau's tache cerebrale (persistence of a red line 
after striking the skin) can usually be elicited. Erythema, urticaria, 
and even gangrene have been observed. The abdomen is often retracted. 
Leukocytosis (25,000 to 40,000) is usually present, and is polynuclear 
in type. Slight albuminuria, rarely glycosuria, may be encountered. 
The bowels are usually constipated. The spleen may be enlarged, but 
often is not demonstrably so. 

Varieties. — The following types may be recognized: Abortive cases, 
in which there are severe initial symptoms, which, however, soon subside, 
and the patient convalesces. Slight cases, in which there is moderate 
fever of slight duration, ill-developed cerebrospinal symptoms of short 
duration, and a rather quick and satisfactory convalescence. Malignant 
or fulminant cases, in which the symptoms are of great severity, and the 
temperature very high (108° F. or more), and in which death results within 
thirty-six or forty-eight hours. Apoplectiform cases, in which the patient 
suddenly becomes unconscious, possibly paralyzed, and soon dies. 



MENINGOCOCCIC INFECTION; CEREBROSPINAL FEVER 89 

Intermittent cases, in which the fever and the other manifestations vary 
much from time to time, remit and intermit. Chronic cases, in which 
the disease lasts for months, relapses and improvements occurring from 
time to time. 

Complications and Sequels. — Complications and sequels are many and 
various. Pneumonia, pleuritis, pericarditis, arthritis, nephritis, and 
parotitis are not infrequent during the height of the disease. The most 
common sequels are optic neuritis and atrophy, parotitis, iritis, and 
panophthalmitis, leading to blindness; otitis media and mastoiditis, 
leading to deafness, and when occurring in young subjects to deaf- 
mutism; paralysis of the different cranial nerves, aphasia, hydrocephalus, 
monoplegia, hemiplegia, etc. 

Diagnosis. — The diagnosis is usually evident from the foregoing 
symptoms. Variability in the intensity of the symptoms from time to 
time is one of the most characteristic phenomena of the disease. With 
a view to confirm the diagnosis, lumbar puncture should be resorted to 
— a three-inch needle with a good-sized caliber being introduced into 
the fourth intervertebral space (just below a line drawn between the 
crests of the ilium). Cytodiagnosis may be resorted to: in cerebro- 
spinal meningitis the polynuclear cells predominate in the exudate, 
whereas in tuberculous meningitis, the mononuclear cells predomi- 
nate. Diplococcus intracellularis meningitidis is also easily demon- 
strated in the exudate by microscopic examination; cultural methods 
and inoculations into lower animals will help to a diagnosis in doubtful 
cases. Usually not much difficulty is experienced in differentiating 
typhoid fever and pneumonia; but in some cases with marked meningism 
the differential diagnosis may be for the moment impossible without 
resort to lumbar puncture, and since this is not only a diagnostic measure, 
but also a therapeutic measure of value, it should not be delayed. Menin- 
gitis, of course, may complicate pneumonia and typhoid fever. 

Prognosis. — The mortality varies much in different epidemics — from 
25 to 75 per cent. — and is usually in direct ratio to the severity of the 
cerebral symptoms. Fulminant cases may result fatally within twelve 
hours ; and ordinary acute cases in from four to ten days. In favorable 
cases convalescence usually sets in at the end of ten to fifteen days, but 
it may be much delayed, and death may eventually result, generally from 
complications or exhaustion, at the end of weeks or even months. 

Treatment. — Isolation and other prophylactic measures (page 29), rest 
in bed, quiet, and a liquid and soft nutritious diet comprise the general 
measures useful in the disease. Flexner's antimeningococcic serum, 
although still on trial, seems to be more or less of a specific. In using 
it, lumbar puncture should be first performed, and then 30 c.c. (in 
fulminant cases, 45 c.c.) of the serum should be injected. This should 
be done daily for four or five days; more frequently, if the symptoms 
are alarming, and for a longer period, if the symptoms persist. The 
use of extract of washed leukocytes has been suggested by Hiss. In 
the absence of a specific, treatment is largely symptomatic. Hydro- 



90 BACTERIAL INFECTIONS 

therapy is of value in most cases, and in addition to a tub bath, should 
the temperature be high, much relief is afforded by an ice-bag to the 
head and along the spine. Hot baths are often grateful to the patient, 
and seem to lead to some improvement in the general symptoms. Counter- 
irritation by means of the Paquelin cautery is much preferable to blisters. 
Preparations of opium are useful in relieving the headache, the pains 
in the back, and the muscular contractions, and may often be serviceably 
combined with atropine or the bromides. Potassium iodide, ergot, 
quinine, salicylic acid, cannabis indica, and mercury (for its antiseptic 
properties) have also been recommended. Pilocarpine has been reported 
of value by reason of the leukocytosis it induces. Stimulants may be used 
when exhaustion supervenes. Lumbar puncture is a very serviceable 
procedure — not only diagnostically but therapeutically. The withdrawal 
of 20 to 30 c.c. of cerebrospinal fluid is often followed immediately by 
relief of the headache and the muscular contractures, and it is reasonable 
to suppose that a certain amount of toxins is also withdrawn. The pro- 
cedure may be repeated from time to time. It has been suggested to irri- 
gate the cerebrospinal canal with physiological saline solution; perhaps 
with improvement in technique this may become a well-indicated thera- 
peutic measure. 

G0N0C0CCIC INFECTION. 

Gonococcic infection is an acute, specific, infectious, and highly con- 
tagious disease caused by Micrococcus gonorrhoeae (Neisser), and charac- 
terized by blenorrhagia and sometimes by general systemic infection. 

Etiology. — The specific cause of the disease is the gonococcus, which, 
although usually acquired in sexual intercourse and attacking first the 
mucous membrane of the urethra in the male, and the vulva, vagina, 
and urethra in the female, may nevertheless attack any mucous membrane, 
such as the conjunctiva, the anus, the oral mucous membrane, etc. 
While the lesions that it provokes are often confined to the genito-urinary 
tract, it not uncommonly causes the most widespread local disease, 
such as cystitis, prostatitis, vesiculitis, epididymitis, orchitis, etc., in the 
male, and endocervicitis, metritis, salpingitis, ovaritis, peritonitis, etc., 
in the female; it is one of the most prolific causes of continued ill-health 
in both sexes, but especially in women the innocent victims of uncured, 
more or less quiescent, antemarital infection in their husbands; and 
it sometimes gives rise to general infection. The general manifesta- 
tions of the local infection are due, in the great majority of cases, to 
toxemia; occasionally, however, to gonococcic bacteremia. Although 
arthritis, endocarditis, pericarditis, myocarditis, myelitis, keratitis, 
iritis, and panophthalmitis, etc., have been reported, special impor- 
tance in the present connection attaches to: (1) Gonococcic bacteremia; 
(2) gonococcic endocarditis; and (3) gonococcic synovitis and arthritis. 

Symptoms. — Gonococcic bacteremia (septicemia, pyemia) has occasion- 
ally been observed in association with a focus of suppuration in the 



GONOCOCCIC INFECTION 91 

genitourinary tract, and with gonococcic endocarditis and arthritis. 
The symptoms have been those of profound intoxication together with 
the manifestations of the local infection. The gonococcus has been 
cultivated from the blood. 

Gonococcic endocarditis has been observed in a few, but gradually 
increasing number of cases. It has usually been associated with (some- 
times preceding, sometimes following) arthritis, and the gonococcus 
has been isolated from the blood; in other words, the condition is a bac- 
teremia. The symptoms do not differ from those of endocarditis due to 
other causes. Pericarditis and myocarditis have been observed in a few 
fatal cases. 

Gonococcic synovitis and arthritis develop usually when the acute 
urethritis is subsiding, occasionally when it has become chronic. It is 
somewhat more common in men than in women. It may involve one 
or several joints; more than one are more frequently involved than is 
generally supposed. The knee (men), wrist (women), and ankle are 
most likely to be attacked, but the smaller joints are not infrequently 
affected. Irregular fugitive pains and possibly some tenderness are com- 
mon during many attacks of gonococcic urethritis, but they are doubtless 
expressions of the toxemia and they soon subside. In other cases the 
more common manifestations of synovitis develop — extreme pain, 
tenderness, swelling, and inability to move the joint. Slight fever may 
be present for several days, but in most cases (in the absence of suppura- 
tion) it soon subsides, and the general symptoms are inconspicuous as 
contrasted with the local. The effusion is within and without the 
joint, and may extend along the fasciae and the tendons and involve 
the bursa?. It is usually serous or serofibrinous in character. By 
aspiration and culture methods the gonococcus may be recovered, but a 
mixed infection is not unknown. Occasionally suppuration results 
(suppurative synovitis, empyema or phlegmon of the joint) and may 
result in widespread destruction of the articulating surfaces. Mild 
infections may result in recovery, but permanent stiffness (fibrous anky- 
losis) due to chronic inflammation of the articular and periarticular 
structures is much more common. Occasionally a chronic hydrops 
(hydrarthrosis) ensues. Bony ankylosis may result from the more 
destructive infections. Exostosis, especially of the os calcis, is not un- 
common, and gives rise to local pain, tenderness, and a " tiptoeing 
gait'*' (one form of "painful heel")- 

Diagnosis. — Gonococcic synovitis and arthritis may be distinguished 
from rheumatic fever (to which it is in no way related) by the history 
of urethritis, severity of the local lesions, relative meagreness of the 
general symptoms, persistence of the articular lesions and their non- 
response to the salicylates, and the more likely involvement of the tem- 
poromaxillary, sternoclavicular, sacroiliac, pubic, and intravertebral 
joints. 

Treatment. — The urethritis, whether acute or chronic, should receive 
attention. The salicylates and potassium iodide are of very little, if 



92 BACTERIAL INFECTIONS 

any, service. Some good seems to attend the use of syrup of iron iodide, 
10 to 60 minims (0.6 to 4 c.c.) three times a day. In most cases tonics 
are called for sooner or later, in which event iron, quinine, strychnine, 
arsenic, and cod-liver oil may be valuable. For the relief of the local 
symptoms nothing is as efficacious as absolute rest enjoined by a fixed 
dressing. All other measures, such as hot and cold applications, lead 
water and laudanum, counterirritation, ointments of ichthyol, bella- 
donna, mercury, iodine, etc., though of value, are of subsidiary impor- 
tance. If the joint has become fixed in a poor position, it must be straight- 
ened, under an anesthetic, if necessary. If improvement is not mani- 
fested soon, the joint should be opened, irrigated, and subsequently treated 
aseptically. Counterirritation (blisters, thermocautery), massage, passive 
movements, superheated dry air ('" baking the joint"), and Bier's " passive 
hyperemia" treatment are sometimes of value in relieving some of the 
chronic manifestations. An antigonococcic serum has been used, with 
indifferent success. Bacterial vaccines seem to have been of service in 



some cases. 



TUBERCULOSIS. 

(Phthisis; Consumption; Scrofula.) 

Tuberculosis is a specific, infectious, and mildly contagious disease 
caused by Bacillus tuberculosis (Koch); it is characterized anatomically 
by the development of small nodules, so-called tubercles, or a diffuse 
productive inflammation, both of which tend to undergo caseation and 
softening or, less commonly, fibrosis and calcification; the clinical mani- 
festations vary, depending upon the type of infection and the tissues 
especially involved.- 

Etiology. — Tuberculosis is an exceedingly widespread disease ; it occurs 
in all parts of the world, although it is most prevalent in the temperate 
zone and at low rather than high altitudes; and it affects many species 
of animals, notably man, cattle, fowls, birds, domestic animals, etc. 
Of human, subjects, no race is exempt; the negro and the American 
Indian display a high degree of susceptibility, and the Hebrew appar- 
ently some relative immunity. The disease occurs at all ages, but there 
seems to be a special susceptibility during the first two years of life 
(perhaps due to milk-borne infection or close association with a tuber- 
culous mother), and during adolescence and early adult life (fifteenth 
to twentieth years). Sex as such is without etiological significance; the 
frequency of the disease in women may be in part attributed to a sedentary 
indoor life, lack of outdoor exercise, pregnancy, and lactation — which 
reduce the resisting powers. The poor and the industrial workers are 
especially subject to the infection; both often are provided with insuffi- 
cient and improper food and clothing; they live and work in dark, 
overcrowded, ill-ventilated, and otherwise insanitary rooms; and they 
are subject often to prolonged and exhausting labor and to the inhalation 
of irritating, dust- and bacilli-laden atmosphere, etc. Other predisposing 



TUBERCULOSIS 93 

factors comprise trauma (especially of the bones and joints); catarrhal 
inflammation of the respiratory tract (often tuberculous from the begin- 
ning); infectious diseases like pneumonia (often tuberculous from the 
beginning), influenza, pertussis, measles, typhoid fever, syphilis, etc.; 
debilitating diseases, such as diabetes, carcinoma, etc.; aneurysm and 
compression of the lung, and chronic diseases of the heart associated 
with anemia of the lungs, such as aortic valve disease: mitral valve 
disease, in consequence of the chronic pulmonary congestion that it 
induces, seems to afford some immunity to tuberculosis of the lungs. 
Some persons seem to possess a more or less efficient natural immunity, 
some of these being descendants of tuberculous ancestors. One attack 
of the disease does not confer immunity, at least not a lasting immunity, 
since recurrences or relapses are the rule. 

The exciting cause of the disease is Bacillus tuberculosis, of which 
four types may be distinguished — the human, the bovine, the avian, and 
the piscian. These, perhaps, originally comprised a single type, but 
owing to environmental conditions have developed special individual 
characteristics. The human and the bovine types are intercommunicable, 
but the avian and the piscian types appear to be either incapable of 
producing tuberculosis in man or capable of producing it only in a mild 
form. Raw has recently suggested that in the human subject the human 
type of the bacillus affects the lungs, the intestines, and the abdominal 
viscera, while the bovine type affects the lymph nodes, the peritoneum, 
the meninges, the bones and joints, and probably the skin — an opinion 
that has not yet been confirmed. Infection is transmitted largely through 
the medium of infected air or infected food; but it may be transmitted 
also by direct contact or inoculation, and perhaps by a third person, by 
fomites, and by domestic animals. The air becomes infected through 
the drying and subsequent dispersion of bacilli-laden sputum, and 
through the projection into the atmosphere by coughing of minute, 
invisible, droplets of infected sputum and saliva. Food, especially 
milk and butter, becomes contaminated by tuberculosis especially of 
the udders of cattle, or by being incautiously handled by tuberculous 
subjects; the meat from tuberculous cattle also may be infected by 
widespread tuberculosis of the animal; and the milk, meat, butter, and 
other foodstuffs may become infected by flies and other insects that have 
walked on or fed upon tuberculous sputum. Infection may be acquired : 
(1) By inhalation — which is doubtless the most common mode of infec- 
tion. The bacilli probably gain access to the tissues through the walls 
of the bronchi or bronchioles, and set up a primary pulmonary tuber- 
culosis. (2) By ingestion — probably the second most common mode 
of infection. The bacilli carried in foodstuffs may penetrate the in- 
testinal mucosa without producing discoverable lesions; thence they 
gain access to the mesenteric lymph nodes, where they may set up tuber- 
culous lesions; or, according to some observers, they invade the thoracic 
lymphatics and from these subsequently involve the lung, giving rise in 
this manner to pulmonary tuberculosis. (3) By way of the tonsils and 



94 BACTERIAL INFECTIONS 

other lymphatics of the oral and pharyngeal cavity (such as carious teeth, 
etc.). Tuberculosis of the cervical lymph nodes ensues, and from these 
foci, dissemination may occur to other parts of the body, especially the 
lungs. (4) Direct inoculation into the skin through an abrasion, as may 
occur at dissections, operations, necropsies, etc.; the ensuing lesion is 
often spoken of as an anatomical tubercle. (5) By direct inoculation 
of the genitalia in sexual intercourse — a rare mode of infection, but per- 
haps responsible for some cases of tuberculosis of the uterus and Fallo- 
pian tubes; rarely of other parts of the genitalia in both sexes. (6) By 
way of the placenta — the foetus becoming infected by a tuberculous 
mother. This so-called congenital tuberculosis is very rare in the 
human subject; it seems to be more common in certain of the lower 
animals, especially cattle. 

Infection having occurred, the bacilli may be disseminated more or 
less widely throughout the body: (1) By way of the lymphatics. This 
is the commonest mode of dissemination, especially in all forms of tuber- 
culosis in children, and in the subacute and chronic pulmonary, intestinal, 
and other types of the disease in adults. (2) By way of the bloodvessels. 
This is the mode of dissemination in miliary tuberculosis, the bacilli 
gaining access to the vascular channels through rupture thereinto of a 
tuberculous focus, most commonly the rupture of a tuberculous bron- 
chial lymph node' into a pulmonary vein. (3) By way of a mucous 
surface. This is a common mode of extension of the lesions in pul- 
monary tuberculosis, infectious material (sputum) being discharged into 
a bronchus and then aspirated into another bronchus that leads to an 
uninvolved portion of the lung; certain intestinal ulcers also perhaps 
exemplify this mode of dissemination, sputum being swallowed and 
infecting the intestinal mucosa. 

Pathology. — Although no organ of the body is exempt from tubercu- 
losis, the incidence of involvement varies considerably. In children, 
the lymph nodes, bones, and joints are most commonly involved; in 
adults, the lungs, intestines, urinary organs, serous membranes, etc. 
The lesions Consist of two main types — tubercle formation and a diffuse 
productive inflammation. The characteristic lesion is the tubercle, 
which in its earliest stage, the so-called miliary tubercle, consists of a 
grayish, somewhat translucent nodule, a millimeter or less in diameter 
(the size of a millet seed) ; it is firmer than the surrounding tissue, projects 
slightly from the general level of the cut surface of an organ, and may be 
delimited by a narrow zone of reactive congestion. In the course of 
time these miliary, or gray, tubercles increase in size by peripheral 
extension, and concurrently therewith their centres become yellowish in 
color and soft — the so-called yellow, or caseous tubercle. In consequence 
of the coalescence of neighboring tubercles, large tuberculous masses 
form and may attain the size of a hen's egg (the so-called solitary tubercle, 
common in the brain and meninges); and in consequence of central 
caseation and liquefaction necrosis, a so-called tuberculous (or cold) 
"abscess" (consisting, however, only of more or less fluid or inspissated 



TUBERCULOSIS 95 

granular debris) results; this being discharged externally leaves a cavity 
(especially common in the lungs), or one or several sinuses (especially 
common in connection with bones and joints). In the neighborhood of 
coalesced tubercles, small gray or yellowish tubercles are usually en- 
countered, the result in most cases of lymphatic extension (so-called 
mother and daughter tubercles). The much rarer diffuse productive 
inflammation may occur in any organ, but is most common in the lungs 
and the lymph nodes. It may or may not be associated with the forma- 
tion of definite tubercles. For instance, the inhalation of large numbers 
of virulent bacilli by susceptible individuals may lead to the rapid 
development of tuberculous pneumonia, which exhibits many clinical 
and pathological analogies with ordinary pneumococcic infection of the 
lung. In the early stages, however, the lung has a more gelatinous 
appearance, due to certain peculiarities of the inflammatory oedema; 
later it becomes cheesy in character, and often the seat of widespread 
softening and excavation. 

The first effect of tubercle bacilli settled and multiplying in the tissues 
appears to be irritative rather than degenerative — proliferation rather 
than death of the cells. The earliest lesions consist of the development 
of large, ovoid, or polygonal cells with ovoid or elliptical, vesicular nuclei, 
and an abundant cytoplasm, harboring usually few or many tubercle 
bacilli. These cells, spoken of as epithelioid or endothelioid, on account 
of obvious resemblances, are derived from proliferation of the endothe- 
lium of capillary bloodvessels and lymphatics, as well as other fixed 
connective tissue cells. About this focus of epithelioid cells (so-called 
epithelioid tubercle) leukocytes collect in greater or less numbers : at first 
many polynuclear cells, but soon mononuclear cells predominate (so- 
called lymphoid tubercle). This cellular accumulation, which does not 
differ from the small round-cell accumulations of inflammation, com- 
prises lymphocytes from the surrounding vascular and lymphatic channels, 
as well as proliferated fixed connective cells ; that is, the chemotactic influ- 
ence of the tubercle toxin seems to be lymphocytic rather than poly- 
nuclear leukocytic. About this time, the capillaries of the tuberculous 
focus become occluded, and since new capillaries are not formed, the 
tubercle soon becomes both extravascular and avascular. In its early 
stages the tubercle may consist only of these epithelioid and lymphoid 
cells, in varying proportion, and a delicate reticulum, doubtless the 
remains of stretched and otherwise altered fibers of the fixed connective 
tissue. In many cases, however, so-called giant cells also are encoun- 
tered: large, irregular cells, with many nuclei arranged peripherally or 
toward one pole, and containing many tubercle bacilli. These result 
from fusion of neighboring epithelioid cells or from nuclear proliferation 
(partly amitotic) without coincident cytoplasmic division. The appear- 
ance within these giant cells of a hyaline or granular centre, as well as 
certain peripheral extensions, suggesting perhaps fusion of adjacent 
epithelioid cells, indicates that the giant cell is the first retrograde 
change within the tubercle. Soon, however, other evidences of necrosis 



96 BACTERIAL INFECTIONS 

supervene — the result of the direct action of the tubercle toxin as well 
as the avascularity: the nuclei of the central epithelioid cells undergo 
various retrograde changes (hyperchromatosis, karyolysis, karyorrhexis, 
pyknosis), the cytoplasm becomes granular (ground-glass appearance), 
and the cell outline becomes indistinct; ultimately all cellular structure 
disappears, and the central portion of the tubercle becomes converted 
into a granular cheesy mass. This necrosis increases by peripheral 
extension, so that ultimately the tubercle consists of a central necrotic 
area, and more or less ill-defined zones of epithelioid cells and giant cells, 
and of round-cell infiltration. In some cases, in consequence of immu- 
nizing processes, caseation becomes retarded or arrested, the peripheral 
fibroblasts are enabled to build up more or less efficient new connective 
tissue, which may or may not contain tubercles, and ultimately the 
tuberculous focus may be surrounded, encapsulated, or pervaded by 
fibrous connective tissue (fibrocaseous tubercle). This fibrosis may 
progress until the tuberculous focus has been completely absorbed, and 
cure ensues; more commonly, perhaps, more or less caseous material 
remains within the connective tissue capsule, and the capsule itself may 
become calcified (quiescent, inactive tuberculosis). In the event of 
progressive caseation, secondary infections are quite likely to ensue, 
especially in the lungs — infections with the pneumococcus, staphylococcus, 
streptococcus, influenza bacillus, Micrococcus tetragenus, etc. The 
general toxemia that results from the absorption of the tubercle toxin 
leads to fever, emaciation, amyloid and fatty degeneration, etc. ; but some 
of the general manifestations, such as the so-called hectic fever, are due 
in part to the toxemia of the secondary infections. 

Acute Miliary Tuberculosis. 

Etiology. — In addition to the general etiological factors, already men- 
tioned, special importance attaches to the predisposing influence in mil- 
iary tuberculosis of : (1) Childhood and youth, perhaps accounted for by 
the great activity of the lymphatic system, especially its active absorp- 
tion and conduction; (2) localized chronic pulmonary tuberculosis, in 
which the fatal termination is frequently determined by dissemination 
of the process (miliary tuberculosis) — in the lungs or more or less widely 
throughout the body; (3) other acute infections, such as pertussis, 
measles, typhoid fever, etc., which are not infrequently followed by 
miliary tuberculosis ; (4) trauma, the mechanical effect of which may be to 
permit the entrance of tubercle bacilli into the blood stream, or to activate 
a quiescent tuberculous focus which later may lead to dissemination of 
the infection; (5) pregnancy, the puerperium, and lactation, which may 
reduce the resisting powers; and (6) debilitating diseases, like diabetes, 
cirrhosis of the liver, chronic nephritis, etc., in which the lethal issue is 
often due to miliary (and other forms of) tuberculosis. 

Pathology. — Acute miliary tuberculosis may be confined to one or 
several organs, or it may be widespread through the body. The infection 



ACUTE MILIARY TUBERCULOSIS 97 

is transmitted by the blood stream, to which the bacilli gain access in 
consequence of, (1) the irruption of a tuberculous focus into the vascular 
stream, or (2) tuberculous disease of the wall of a vein, artery, or lymph 
vessel. The characteristic lesion consists of the miliary or gray tubercle; 
but in some cases, of comparatively slow progression or moderately long 
duration, more or less caseation, the so-called yellow tubercle develops. 
These tubercles, especially the miliary or gray tubercle, may be found 
in any organ or tissue of the body, but they are most common in the lungs, 
liver, spleen, kidneys, intestine, meninges, etc. If, as is common, there 
is primary disease of the lungs or the peribronchial lymph nodes, the 
bacilli may gain entrance into the pulmonary veins, and be thence trans- 
mitted to the heart and the systemic circulation. In other cases, the 
bacilli may gain the blood stream by way of the thoracic duct. In cases 
of disseminated infection, tuberculous arteritis, phlebitis, and lymphan- 
gitis have been found, but it is not always possible to determine whether 
these vascular lesions are the result or the cause of the generalized disease; 
older lesions in the vessel walls, however, suggest that they are the ante- 
cedent process. Tubercles have been found in the walls of the thoracic 
duct, the pulmonary veins, the jugular veins, the aorta, and certain 
smaller arteries, etc. In the lungs miliary tubercles are usually present 
in greatest numbers, and are likely to be most widespread in distribution ; 
they may develop in the alveolar walls or in the peribronchial or peri- 
vascular tissues. The liver is almost always affected in generalized 
miliary tuberculosis; two sources of infection are possible — the portal 
and the general arterial circulatory system; the tubercles may be found 
in the intralobular or interlobular tissue, and there may be also some 
hyperplasia of the connective tissue and proliferation of the biliary ducts. 
In the spleen the tubercles may be distributed regularly or irregularly. 
In the walls of the intestine tubercles are common, especially in the 
submucous and serous coats, and they are usually associated with adja- 
cent ulceration. Infection may occur through the lumen of the gut or by 
way of the blood stream. In the kidneys, which are commonly involved, 
the tubercles are most frequently seen in the cortex. The serous mem- 
branes, notably the cerebrospinal meninges, the peritoneum, the pleurae, 
and the pericardium, are commonly involved; occasionally also the endo- 
cardium. The tubercles develop also in the bone marrow, the choroid 
coat of the eye, etc., but they seem to be comparatively uncommon in the 
pancreas, thyroid body, the myocardium, the stomach, the uterus, etc. 

Symptoms. — The symptoms vary considerably in different cases. In 
the one series of cases, following a more or less obvious tuberculous focus 
somewhere in the body (lungs, lymph nodes, testicles, bones, joints, etc.), 
evidences of general involvement of the body develop — the so-called 
general, typhoid, or toxic form; in another series, the major symptoms 
are referable to the lungs — the so-called pulmonary form; and in still 
another series, the chief phenomena are cerebral — the so-called menin- 
geal form; bu,t in most cases the lesions are more or less widespread, 
7 



98 BACTERIAL INFECTIONS 

although the predominant symptoms may be referable to one or 
another system of organs. 

In cases without an obvious antecedent tuberculous focus somewhere 
in the body, the first noteworthy symptoms consist, as a rule, of general 
failure of the health, weakness, anorexia, and fever. The fever may be 
continuous in type, or from time to time remittent. 

In pulmonary infection, the sudden development of high tempera- 
ture running continuously over an extended period is always suggestive 
of the development of miliary tuberculosis. The irruption of the in- 
fectious material into the blood doubtless marks the inception of the 
pyretic condition. The temperature may reach 104° or 105° F.; there 
is usually a drop of 1° or 2° in the morning temperature, but now and 
then this may be reversed, the evening temperature being the lower, 
which by some observers has been held to be diagnostic of the disease. 
Although the majority of cases present fever of one or another type, some 
show a continuously subnormal temperature; some of these may be 
interpreted as cases of cerebral infection, in consequence of which 
depression of the thermogenic centres has taken place. On the contrary, 
others show no such involvement, the absence of fever seeming to be an 
expression of insensibility of the heat-producing centres. 

Certain respiratory symptoms, such as dyspnoea, cough, and cyanosis, 
are quite constant. Dyspnoea may be intense, especially in children, a 
respiratory rate of 75 to 90 per minute not being unusual. This is pro- 
duced not infrequently without especial lung involvement, in which event 
it has been ascribed to a toxic condition of the respiratory centres and to 
the development of tubercles on the diaphragm. Miliary tubercles in 
the pulmonary tissues may be sufficiently irritating to exert a pro- 
nounced effect upon the pneumogastric nerve. Cheyne-Stokes breathing 
is not infrequently observed. Dyspnoea and increase of pulse rate are 
usually coincident in their development, but not rarely dyspnoea has the 
precedence. Cough is an important symptom, preceding not infre- 
quently the development of dyspnoea. It is probably due to the toxemia, 
as well as to the mechanical effect of the tubercles in the lungs. It is 
variable in its intensity, some cases presenting a violent paroxysmal 
cough which, when associated with severe dyspnoea, simulates asthma. 
In the early stages of the affection there is little, if any, expectoration, 
but now and then small quantities of blood may appear. This rarely is 
in such quantities as to resemble the rusty sputum of croupous pneu- 
monia. In the later stages, the expectoration is more abundant and 
becomes mucopurulent in character. This picture is somewhat altered 
when there has been an antecedent chronic pulmonary tuberculosis, 
and the acute generalized condition is a complication. Under these 
circumstances the dyspnoea and cough usually have existed for an ex- 
tended period, and there is usually an exaggeration of the symptoms 
upon the development of the additional infection. Cyanosis may be 
extreme, more so than in most other diseases, and is quite significant of 



ACUTE MILIARY TUBERCULOSIS 99 

miliary tuberculosis of the lungs (eliminating emphysema and pneu- 
monia) . 

The cardiovascular system is more or less affected. The heart action 
becomes accelerated, the sounds become weak, and passive congestion 
and oedema of the dependent parts mark the later stages of the disease. 
The blood pressure is typically lowered. The pulse is quickened, 
averaging 120 to 150 beats per minute, and at times is dicrotic in char- 
acter. The greatest acceleration of pulse rate is seen in children, while 
in the aged it may be below 100 per minute. 

Anorexia is constant, and nausea and vomiting are often present, 
especially in meningeal infection. Abdominal tenderness and meteor- 
ism are at times noted, especially in the presence of peritonitis. The 
patient is usually constipated, though diarrhoea may occur from time to 
time, and be associated with hemorrhage, with or without intestinal 
ulceration. The amount of urine excreted is usually small, the result 
in part of profuse sweating, especially at night. In practically all cases 
there is a low-grade nephritis which accounts for a slight albuminuria. 
Peptonuria and excessive excretion of urates often accompany the disease. 

The skin generally is pale, but in the peripheral portion of the body, 
as the fingers and toes, more or less, sometimes extreme, cyanosis is evi- 
dent. Eruptions of several types are sometimes seen, such as herpes, 
petechias, miliaria, sudamina, etc. Miliary tubercles are rare cutaneous 
lesions. Profuse sweating occurs in practically all cases, and is due to 
a toxic effect upon the nervous system. This generally appears at night 
and is coincident with a fall of temperature. 

Certain nervous symptoms are seen in almost all cases of generalized 
miliary tuberculosis without meningeal involvement, such as headache, 
vertigo, hebetude, and somnolence; they are referable to the toxemia. 
The headache may be mild or severe, frontal or vertical in type. It is 
usually most marked during the periods of increment of fever. Vertigo 
is usually not so conspicuous unless there is meningeal infection. Hebe- 
tude and somnolence are often marked in the later stages. When 
meningeal infection is present the nervous symptoms are intense and 
tend to overshadow the general symptoms, such as cough, dyspnoea, 
profuse sweating, etc. Convulsions, paralyses, vomiting, painful con- 
tracture of the posterior cervical muscles, strabismus, contraction or 
dilatation of the pupils, and flexion-contracture of the knee (Kernig's 
sign) may occur. Delirium, coma, and death often terminate the condi- 
tion. Tubercles may develop in the choroid coat, usually of both eyes. 

Physical Signs. — The physical signs, as a rule, are merely those of 
bronchitis, although, of course, in some cases they are modified by the 
signs of antecedent pulmonary tuberculosis, such as solidification or 
cavity formation. The percussion note may be somewhat hyperresonant 
— from inflation of the lungs. The breath sounds are harsh and the 
expiration prolonged; the rales may be fine crackling or bubbling, or 
sibilant and sonorous; frictions may be heard (pleural tubercles). In 
the course of time, a soft systolic murmur may become audible at the 



100 BACTERIAL INFECTIONS 

apex of the heart, and the pulmonary second sound may become accen- 
tuated (congestion of the lungs). The liver and the spleen are some- 
times moderately enlarged from congestion and the presence of tubercles ; 
they are rarely tender. Meteorism, abdominal tenderness, and rigidity 
are often seen in involvement of the peritoneum. 

Diagnosis. — The pulmonary form of miliary tuberculosis is usually 
readily recognized from the detection of an antecedent tuberculous 
focus in the lungs or elsewhere, the presence of cough, dyspnoea, marked 
cyanosis, the physical signs of bronchitis, and tubercle bacilli in the 
sputum (which, however, may be missed until late in the course of the 
disease). Cerebral symptoms suggest meningeal involvement, which 
may be determined definitely by finding tubercle bacilli and an excess 
of lymphocytes in the cerebrospinal fluid, or by detecting choroid tuber- 
cles. The general, toxic, or typhoid form resembles and is commonly 
mistaken for typhoid fever, but its likelihood is suggested by absence 
of the characteristic typhoid fever curve, of abdominal symptoms, of 
erythematous rose-spots, of leukopenia, and of the Gruber-Widal reac- 
tion, and by the presence of increased pulse rate, of dyspnoea, of cyanosis, 
of occasionally bloody sputum, of choroid tubercles, and of tubercle 
bacilli in the cerebrospinal fluid and rarely in the blood. 

Prognosis. — The outlook is extremely grave; so far as is known the 
termination is invariably fatal in from a few hours (apparently) to 
several weeks or several months. The average duration of the general 
or typhoid cases is about four weeks; that of the meningeal cases some- 
what less. 

Tuberculosis of the Lymphatic System. 

Lymph Nodes. — Etiology. — Tuberculosis of the lymph nodes (scrof- 
ula) is very common in children, especially prior to the tenth year 
of age, and in the female sex; but it may occur in both sexes and at 
all ages. The process may be widespread or circumscribed, especially 
to the cervical, bronchial, or mesenteric lymph nodes. In the cervical 
cases the infection occurs by way of the tonsils, carious teeth, and the 
cutaneous and mucous surfaces of the head and neck and related cavities 
(nose, mouth, pharynx, larynx, etc.). The bronchial nodes are involved 
in all cases of pulmonary infection, in adults as well as in children; the 
infection may be bronchogenic, or, especially in children, it may occur 
by way of the intestine, the bacilli penetrating the mucosa and traversing 
without infecting the mesenteric and other abdominal lymph nodes. 
Some writers maintain that in many of these cases infection occurs 
during intra-uterine life, and that there is a variable period of latency or 
quiescence after birth. The mesenteric and retroperitoneal nodes may 
become infected in consequence of infected food, especially milk and 
butter; the disorder is especially common in children (tabes mesenterica). 
In adults mesenteric involvement is commonly secondary to intestinal 
ulceration. 



TUBERCULOSIS OF THE LYMPHATIC SYSTEM 101 

Pathology. — The lesions consist of tubercle formation, at first gray 
or miliary tubercles, and later yellow or caseous tubercles; or of diffuse 
productive inflammation. The diseased lymph nodes vary in size from 
that of a pea to that of a walnut or thereabout. Usually one node after 
another in a chain becomes diseased. At first they are firm and flesh-like, 
but generally, especially in the neck, they undergo caseation, softening, 
and may discharge externally. Like changes may occur in other situa- 
tions. On the other hand, there is some considerable tendency to spon- 
taneous healing, although it may be long delayed; but fibrosis and calci- 
fication often eventually ensue, especially in the bronchial and mesenteric 
nodes. In many of these, notably the bronchial nodes, the tuberculous 
process is merely latent or quiescent, and at a favorable opportunity 
may serve as the source of a more or less widespread infection. 

Symptoms. — On account of their comparatively superficial position, 
tuberculosis of the cervical lymph nodes is readily recognized. Node 
after node, as a rule, gradually increases in size, until the whole chain 
may be involved. Usually there is little, if any, pain, especially in the 
early stages; tenderness, as a rule, is slight, but from time to time an acute 
exacerbation of the condition may supervene, and lead to increased 
tenderness, some pain, and perhaps redness of the overlying skin: this 
is likely to be associated with an acute infection of the upper respira- 
tory tract (coryza, laryngitis, bronchitis). The enlarged lymph nodes 
manifest a marked tendency toward fusion of adjacent nodes, caseation 
and softening, adhesion with the overlying skin, and the eventual dis- 
charge externally of the caseous material; sinuses may persist for a long- 
time, and may ultimately heal with more or less disfiguring scars. In 
some cases, however, the nodes having reached the size of a bean or 
cherry, gradually decrease in size and become firm and hard; the process 
becomes quiescent, arrested, or healed. Tuberculosis of the bronchial 
nodes may give rise to no symptoms; it is an extraordinarily common, 
almost constant, condition at the necropsy. Sometimes, however, suffi- 
cient enlargement occurs to cause cough (which may simulate that of 
pertussis), dyspnoea, secondary anemia, and more or less impairment 
of the general health. The superficial veins of the chest, neck, and head 
may become distended from interference with the venous circulation in 
the thorax; there may be relative dulness over and to both sides of the 
fifth and sixth vertebrae (de la Camp's sign) and perhaps tenderness 
in the interscapular region (Petruschky's spinalgia); unilateral restriction 
of the respiratory excursions (Grancher's sign) may be present; and in 
some cases if the head is strongly flexed backward a murmur may be- 
come audible over the sternum or in the suprasternal fossa (Eustace 
Smith's sign), supposed to result from compression of the aorta by the 
enlarged lymph nodes. The axillary and inguinal nodes present changes 
analogous to those of the cervical. In localized tuberculosis of the lymph 
nodes, constitutional disturbances are commonly slight, and consist of 
occasional slight fever, increased pulse-rate, and perhaps some loss of 
flesh and strength; in the event of softening, secondary infection, and 



102 BACTERIAL INFECTIONS 

generalization of the process, these general manifestations are likely to 
become marked. In involvement of the mesenteric nodes (tabes mes- 
enterica), loss of flesh and strength, secondary anemia, and debility 
usually become aggravated; the abdomen commonly becomes distended; 
there may be considerable diarrhoea ; and the enlarged nodes may be 
palpable through the abdominal wall. In a few cases, tuberculosis of 
the peritoneum becomes associated. 

Diagnosis. — Tuberculosis must be distinguished from other forms of 
enlarged lymph nodes, especially syphilis, leukemia, benign and malig- 
nant lymphoma, and Hodgkin's disease. 

Prognosis. — Tuberculosis of the lymph nodes is a chronic disorder, 
with a general tendency toward spontaneous recovery — which, however, 
may be delayed by softening and suppuration. Death may ensue if the 
process becomes generalized or the general health seriously impaired. 
The more or less quiescent processes common in the bronchial nodes 
often, when the subject loses his resisting power, are the source whence 
pulmonary and more widespread tuberculosis takes its origin. 

Treatment. — In addition to the general measures to be presently men- 
tioned, enlarged, but especially enlarging and softened, lymph nodes 
should be removed surgically, care being exercised not to handle roughly 
or rupture the softened nodes and thus favor dissemination of the process 
or its local implantation in tissues unaffected. 

Spleen. — Infection of the spleen is usually hematogenic. The common 
lesion is the miliary or the caseous tubercle, although, especially in chil- 
dren, larger caseous masses may develop; these may become calcified. 
The organ becomes only slightly enlarged. In chronic suppurating tuber- 
culosis (secondary infections), especially of the bones, amyloid disease 
of the spleen is likely to develop and give rise to notable enlargement 
of the organ, which may be readily detected upon physical examination. 

Bone Marrow. — Miliary tuberculosis of the bone marrow occurs in 
practically all cases of generalized miliary tuberculosis, and in some 
cases in which otherwise only the lungs appear to be involved. The 
infection is hematogenic. In advanced tuberculosis of other organs, the 
bone marrow is frequently soft and gelatinous. The bone marrow may 
also become involved by extension of tuberculosis of the epiphysis or 
other parts of the bone, whereupon caseous masses are likely to develop. 

Serous Membranes. — Pleura. — Tuberculosis of the pleura rarely 
perhaps may be primary, though this is doubtful ; usually it is secondary 
to disease of the lungs or bronchial lymph nodes, or it may follow dis- 
ease of the vertebrae, pericardium, peritoneum, etc. It may occur in an 
acute or a chronic form. The acute cases are represented by the majority 
of the cases of ordinary serofibrinous pleuritis (which upon good evidence 
are properly viewed as tuberculous, although this may be demonstrable 
only upon finding tubercle bacilli in the exudate, by cultural experiments 
or animal inoculations, or by demonstrating lymphocytosis of the exu- 
date); in other cases, miliary tubercles may be present — usually asso- 
ciated with generalized miliary tuberculosis. In the chronic cases, the 



TUBERCULOSIS OF THE LYMPHATIC SYSTEM 103 

pleura may be greatly thickened with fibrous or fibrocaseous tissue; or 
dense adhesions may bind together the two serous surfaces so that the 
pleural sac is obliterated; or rarely large caseous masses, analogous to 
the "pearl disease" of cattle, may develop. Rupture into the pleural 
sac of a tuberculous cavity and the establishment of a communication 
between the respiratory tract and the pleura is the commonest mode of 
development of pneumothorax or pyopneumothorax. These conditions 
are discussed in detail under diseases of the respiratory system. 

Pericardium. — Tuberculosis of the pericardium is less common than 
that of other serous membranes ; but it is more common than tuberculosis 
of the myocardium or endocardium. The infection is usually lympho- 
genic — from the bronchial lymph nodes; but it may be due to extension 
from the pleura or the mediastinal or other neighboring tissues; and it 
is rarely the result of hemogenic infection. The process may appear 
as: (1) The ordinary serofibrinous pericarditis, which like the similar 
process in the pleura is usually tuberculous; (2) miliary tubercles- -due 
to hemogenic infection; (3) large caseous masses — commonly lympho- 
genic infection; and (4) dense fibrous or fibrocaseous adhesions 
binding together the two serous surfaces and more or less completely 
obliterating the pericardial sac. These conditions are discussed in more 
detail under diseases of the pericardium. 

Peritoneum. — Cases of primary tuberculosis of the peritoneum have 
been reported, but it is exceedingly doubtful if this ever occurs. The 
process is usually secondary to tuberculosis of the pleura, pericardium, 
mesenteric nodes, intestines, genitalia, especially in the female (the 
Fallopian tubes, etc.); and it may be part of a generalized miliary tuber- 
culosis. The infection may occur by direct extension, by continuity 
or contiguity of tissue; or it may be lymphogenic or hemogenic. The 
lesions may consist of miliary tubercles, of larger caseous masses, or 
of adhesions. 

In the miliary type the tubercles are found disseminated more or less 
generally over the peritoneum; they are commonly most numerous over 
the intestines, but they may be seen over the spleen, liver, stomach, pelvic 
organs, and parietal peritoneum. Those miliary tubercles, which are 
found upon the serous surface of intestinal ulcers and not otherwise in 
the peritoneum, are commonly not considered as manifestations of tuber- 
culous peritonitis. A large serous exudate is usually the characteristic 
feature; in some cases the fluid is hemorrhagic in character. The 
caseous or ulcerative type is a chronic condition, and may be the result 
of any of the sources of infection except the blood channels. In this type 
large cheesy masses develop, a plastic exudate is thrown out and gives 
rise to more or less adhesion of the abdominal organs. The omentum 
shares in the condition, and large caseous masses may develop therein. 
The adhesive type is even more chronic, and is characterized by the 
development of dense fibrous adhesions between the various organs. 
There is sometimes an absence of exudate, whence the condition is spoken 
of as dry peritonitis; often there are sacculations with more or less fluid. 



104 BACTERIAL INFECTIONS 

Symptoms. — Miliary tuberculosis of the peritoneum presents the 
usual symptoms of acute generalized miliary tuberculosis, such as fever, 
increased pulse and respiratory rate, headache, loss of appetite, and 
progressive emaciation. Certain localizing symptoms, however, may 
be observed, such as abdominal pain and tenderness, distention, tym- 
panites, and ascites. The bowels may be constipated or loose. The 
onset of symptoms is usually gradual, though in some cases it is abrupt. 
The course is commonly not prolonged beyond one or two months. In 
chronic caseous peritonitis the onset is much more gradual. The patient 
slowly fails in health, emaciates, and develops moderate fever. After 
a time abdominal pain is complained of and tenderness and distention 
are noted. Nausea and vomiting usually appear late in the disease. 
Owing to the wasting of the abdominal tissues and to the obstruction 
offered to the circulation in the intra-abdominal vessels, the superficial 
abdominal veins become prominent. Inflammatory changes about the 
umbilicus with a discharge of purulent or fecal matter may occur. Pal- 
pation reveals a doughiness of the abdomen, marked here and there by 
rather firm tumor-like masses, which have been found to be made up of 
intestinal coils and omentum, sometimes enclosing sacculated fluid. 
The course of the disease may be prolonged over many months and may 
develop into the adhesive type. In the caseous type there are usually 
symptoms referable to infection of other parts of the body, as, for example, 
the lungs and intestines. In many instances the adhesive type is second- 
ary to the miliary or caseous, but some cases are doubtless primary in 
character. The symptoms are much like those just mentioned, except 
that there may be no evidences of abdominal distention and ascites; on 
the contrary, the abdominal walls are likely to be retracted. Pain 
and tenderness are moderate, and constipation is usually marked. 
Tuberculosis of the peritoneum is not infrequently associated with hepatic 
cirrhosis, which is usually the primary condition. 

Diagnosis. — The diagnosis of peritoneal tuberculosis is often diffi- 
cult. In cases of acute generalized disease, which present abdominal 
tenderness, distention, and ascites, the diagnosis is suggested, though 
not infrequently the condition has been mistaken for typhoid fever; in 
the chronic caseous and fibrous types the symptoms and physical signs 
may lead to confusion with simple peritonitis. The fever is likely to 
be more irregular in tuberculosis than in typhoid fever, and it does not 
show the lysis which is characteristic of the latter affection. Abdominal 
tenderness is more commonly general in tuberculosis of the peritoneum, 
while in typhoid fever it is likely to be confined to the cecal region. The 
redness and induration of the tissues about the umbilicus with the dis- 
charge of purulent or fecal material therefrom is diagnostic of tubercu- 
lous peritonitis. Palpation and percussion of the abdomen usually 
reveal masses of omental and intestinal tissues. In many instances it 
may be very difficult to differentiate the simple from the tuberculous 
type of peritonitis. Fluid may be withdrawn from the abdomen, but it 
usually does not show the presence of tubercle bacilli; but may reveal 



TUBERCULOSIS OF THE LYMPHATIC SYSTEM 105 

lymphocytosis. Animal inoculation of this fluid, however, may reveal 
the character of the disease. The detection of tuberculous foci in other 
parts of the body may be of great assistance in the diagnosis of the peri- 
toneal condition. 

Prognosis. — The prognosis depends largely upon the degree of infec- 
tion of other parts of the body, as for example, if the intestines and lungs 
are markedly diseased the outlook is grave. Aside from this, tuberculosis 
of the peritoneum not infrequently becomes spontaneously arrested, its 
specific character disappearing and dense fibrous adhesions developing. 
Cases of miliary tuberculosis of the peritoneum are generally fatal, but 
those of the caseous and adhesive types may undergo a certain degree of 
resolution. The more there is of fibrous tissue and the less of caseation 
the greater is the probability of recovery from the immediate effects of 
the disease. The development of fibrous adhesions may cause consider- 
able disturbance in the functions of the abdominal organs; and relapses 
are not uncommon in those cases, which seem to be tending toward 
recovery. In such an event death not infrequently occurs. Tuberculosis 
of the peritoneum usually warrants a more favorable prognosis than 
tuberculosis of the meninges, and oftentimes of the pleura. 

Treatment. — In addition to the general measures, to be presently 
mentioned, operative procedures are often of much service, although they 
should not be lightly undertaken, since many cases after the lapse of 
several months tend to spontaneous recovery. Recovery also sometimes 
follows repeated tappings. Yeo speaks highly of iodoform, \ grain (0.03 
gram) in cod-liver oil, 2 drams (8 c.c.) thrice daily; and inunctions of 
the abdomen twice daily with a mixture of equal parts of iodoform 
ointment and cod-liver oil. Cceliotomy with or without peritoneal irri- 
gation with physiological saline solution or mild antiseptic solutions, or 
the use of iodoform or other dusting powders, is much superior to simple 
paracentesis. Although the operation is frequently followed by excellent 
results — cure in from one-half to three-fourths of the cases — its mode of 
action is not definitely known : the access of sunlight and air, the trau- 
matism of the operative manipulations, the access of fresh blood serum 
with augmented antitoxic or bactericidal properties permitted by removal 
of the peritoneal fluid, etc., have been credited with the curative properties. 

Tuberculosis of Several Serous Membranes; Multiple Serositis; Polyor- 
rhomenitis. — The pleurae, pericardium, and peritoneum may be involved 
concurrently in tuberculosis, the infection developing simultaneously or 
sequentially in two or more of the serous membranes; and the lesions 
may be equal or disproportionately more marked in the one than in the 
others. They may consist of miliary tubercles, of larger caseous masses 
with more or less fluid exudation, or of fibrous or fibrocaseous thicken- 
ings and adhesions with varying amounts of fluid, sometimes very little, 
sometimes considerable. The condition is discussed in more detail under 
diseases of the peritoneum. 



106 BACTERIAL INFECTIONS 



Tuberculosis of the Circulatory System. 

Heart. — Tuberculosis of the myocardium is rare; it is always sec- 
ondary to a focus elsewhere in the body. Four forms are recognized: 
(1) Miliary tubercles, (2) large caseous tubercles, (3) diffuse tuberculous 
infiltration, and (4) generalized fibrosis. The first three types are usually 
recognized grossly, but the fourth may be evident only upon micro- 
scopic examination. The heart muscle may be involved secondarily 
to the pericardium. The auricular and ventricular walls are involved 
apparently with equal frequency. The lesions of the first type are 
ascribed to blood infection, and the second to dissemination through the 
lymphatics. There are no symptoms by which the disease can be 
diagnosticated; rapid and irregular heart action and sudden death have 
been noted in certain cases, but there are no symptoms which may not 
be referable to simple myocarditis. Tuberculosis of the endocardium 
may appear as valvular vegetations, miliary tubercles over the mural 
endocardium, or diffuse sclerosis of the endocardium. The affection is 
rare, though somewhat more frequent than myocardial tuberculosis. 
It is always associated with acute generalized miliary tuberculosis, and 
the infection naturally reaches the parts through the blood stream. 
Cardiac thrombi have been found to contain tubercle bacilli without 
endocardial lesions being present. There are no symptoms diagnostic 
of the disease; if the valves are affected a murmur may be heard, but 
this may be ascribed to a simple endocarditis. 

Bloodvessels. — The bloodvessels are sometimes the seat of tuber- 
culosis. The aorta is rarely involved as a result of extension from a 
caseous bronchial or mediastinal lymph node; the pulmonary veins may 
contain tubercles in their walls, especially in pulmonary tuberculosis; 
and the small arteries or veins or the capillaries throughout the body 
may reveal miliary tubercles, especially in miliary tuberculosis. Mili- 
ary tuberculosis itself is the result of the irruption into a bloodvessel of 
a tuberculous focus somewhere in the body. In cavity formation in 
the lung, larger or smaller vessels are not uncommonly relatively un- 
affected, even after extensive disease of the other pulmonary tissues; but 
eventually, from primary involvement of the adventitia, the wall becomes 
weakened, bulges (that is, a small aneurysm develops), and may finally 
rupture and give rise to a more or less copious hemorrhage. 

Tuberculosis of the Respiratory System. 

Nose. — Tuberculosis of the nasal mucous membrane is usually 
secondary to a lesion of the lungs or larynx, but a primary focus may 
be the result of infection by means of a contaminated handkerchief or 
finger. The disease may appear in one of two forms, as an ulcer or 
as a tumor-like mass (tuberculoma). Both are rare and practically of 
equal frequency. Lupus involving the face may by continuity of struc- 



TUBERCULOSIS OF THE RESPIRATORY SYSTEM 107 

ture invade the nose. Aside from constitutional treatment, such agents 
may be employed as are capable of destroying the infected tissues, the 
curette and the galvanocautery. 

Larynx. — Primary laryngeal tuberculosis is very rare; many writers 
doubt its existence. Statistics show that it complicates pulmonary 
tuberculosis in 25 to 30 per cent, of the cases. It may appear early in 
the course of the lung disease, but more frequently it is seen at a later 
period. Infection may occur through the respiratory tract, the blood, 
or the lymph. If the condition is primary, the infectious material has 
found its way to the part through the inspired air. In the majority of 
cases of secondary laryngeal infection, those attending pulmonary dis- 
ease, the sputum probably serves as the infectious medium. The fre- 
quency of involvement of the posterior surface of the larynx suggests the 
probability of sputum infection, especially in bedridden patients. The 
blood may be the carrier of infection in cases of generalized miliary 
tuberculosis, while the lymph may act in a similar capacity when there 
is tuberculosis of adjacent structures. Any portion of the larynx may 
become affected. Some statistics show that the vocal cords are more 
frequently diseased than other parts; others show that the epiglottis is 
the commonest seat. The disease appears primarily as a miliary tuber- 
culosis of the subepithelial tissues; after a time coalescence of the lesions 
occurs with more or less erosion of the superficial structures, and ulcera- 
tion results. These lesions usually have a rough, worm-eaten appear- 
ance and are situated rather superficially. On the contrary, tumor 
masses (tuberculomas) may appear, and project into the lumen of the 
larynx. 

Symptoms. — The chief symptoms are hoarseness, pain, difficulty in 
swallowing, and cough. Hoarseness is usually the earliest symptom, and 
gradually progresses to almost complete aphonia, which develops in conse- 
quence of oedema or destruction of the vocal cords. Pain, which usually 
does not appear until late in the disease, may be moderate or severe, 
spontaneous or produced only upon swallowing. In the majority of 
cases cough is produced by the pulmonary lesions, although irritation of 
the laryngeal nerves alone may incite cough. 

Diagnosis. — The diagnosis is readily made in most cases by a direct 
examination of the parts; but syphilitic and malignant ulceration must 
be excluded. The worm-eaten and superficial character of the ulcers 
and the pallor of the tissues are characteristic of tuberculosis; in syphilis 
the destruction of the part is much more rapid, there are evidences of 
inflammation in the surrounding tissues, and the ulceration, which is 
usually solitary, is likely to be deep. Malignancy characteristically 
appears later in life than does tuberculosis and syphilis ; the lesions are 
primarily unilateral in position; and marked cedema and inflammatory 
changes about the ulcer are usually found. 

Prognosis. — The prognosis depends upon the extent of laryngeal and 
pulmonary involvement. A larger percentage of cures is now effected 
than formerly, owing to perfected methods of local treatment. 



108 BACTERIAL INFECTIONS 

Treatment. — Constitutional as well as local measures are important 
in the treatment of this condition. Much can be done for the early 
cases of laryngeal disease, but in those in which extensive destruction of 
the tissues has occurred nothing but a fatal issue is to be expected. 
Subjects who experience severe pains upon swallowing die not infre- 
quently of inanition. The most efficient treatment is that of tubercu- 
losis in general (to be presently mentioned) and the judicious admin- 
istration of such drugs as strychnine, nux vomica, pepsin, creosote, 
and ammonium chloride, etc. Creosote is of value if mixed infec- 
tion is present in the lungs (shown by cavitation and free expecto- 
ration of purulent material). Ammonium chloride (by its stimulating 
properties) is of service in order to alleviate the marked dryness of 
the mucous membrane. The local treatment should consist of the 
application of lactic acid, in a 20 to 80 per cent, solution, to the ulcers. 
Methylene blue in 2 to 4 per cent, solution, or the colloidal silver 
salts in 20 to 30 per cent, solution, may be effective. The curette may 
also be of service. If the condition is far advanced and the patient 
suffers to a marked degree, sedative applications may be employed, such 
as cocaine, boric acid, morphine, iodoform, orthoform lozenges, etc. 

Trachea and Bronchi. — Tuberculous ulceration of the trachea 
and bronchi is not infrequently seen in cases of pulmonary and laryn- 
geal infection. The ulcers are usually small and multiple. The bron- 
chial lesions are more frequently seen in the chronic than in the acute 
form of pulmonary tuberculosis. The ulcers resemble those of the 
larynx in being rather superficial and worm-eaten in appearance. Infec- 
tion in most cases is aerogenous or bronchogenic in character. 

Lungs. — Etiology.— Pulmonary tuberculosis is the commonest mani- 
festation of the disease. Two pathways of infection are postulated: 
the respiratory and the alimentary; but the former is the more generally 
accepted. The respiratory or aerogenous theory presupposes the aspira- 
tion of infectious material into the lower respiratory tract, where it 
becomes deposited upon the mucous surfaces. Direct penetration of the 
bacilli to the alveoli is questionable; it seems probable that they find 
lodgment upon the mucosa of the small bronchi and bronchioles, 
whence they are carried either by the lymph or by phagocytes through 
the mucous membrane to the peribronchial lymph spaces in which the 
primary tubercles develop. From these areas dissemination occurs to 
other parts of the lungs. The alimentary theory 7 presupposes that the 
ingestion of infectious material is followed by the penetration of the 
intestinal walls by the tubercle bacilli and by their convection to the 
mesenteric nodes; thence they pass to the lungs by way of the thoracic 
duct, the left subclavian vein, the superior vena cava, the heart, and the 
pulmonary artery; capillary embolism occurs in the lungs and miliary 
tubercles develop. The majority of cases of pulmonary tuberculosis 
is due to respiratory infection, but a certain number may be the result 
of alimentary infection, especially in children, to whom milk may be a 
frequent carrier of the bacilli. The most important source of pulmonary 



TUBERCULOSIS OF THE RESPIRATORY SYSTEM 109 

tuberculosis is the inhalation of tubercle bacilli brought about by the 
inspissation and pulverization of sputum from a tuberculous patient. 

Pathology. — Tuberculosis of the lungs may develop in one of four 
forms: (1) Acute miliary tuberculosis (which has already been dis- 
cussed); (2) acute pneumonic tuberculosis; (3) chronic ulcerative tuber- 
culosis; and (4) chronic fibroid tuberculosis. 

Acute Pneumonic Tuberculosis. — Acute pneumonic tuberculosis 
occurs in two subtypes — the so-called pneumonic and the bronchopneu- 
monia The so-called pneumonic form is most common in adults, and 
usually involves a lobe or an entire lung. In general the appearances 
are much like those of pneumococcic infection of the lung (croupous 
pneumonia); but in the early stages there is more fluid exudation that 
gives rise to a peculiar gelatinous appearance, and there is likely to be 
less fibrinous exudation and more desquamative changes. Definite 
tubercle formation may or may not be present; in some cases the entire 
exudation consists of the ordinary inflammatory products with marked 
proliferation of the alveolar epithelium, all of which proceeds soon to 
extensive caseation and softening; in other cases, amidst the widespread 
caseation tubercles also may be found. The bronchopneumonic form 
is most common in children and young adults. The lesions consist of 
reddish, later grayish or yellowish foci of bronchopneumonia, which by 
fusion may lead to involvement of almost if not quite all of a lobe or an 
entire lung. There is a marked disposition to caseation, and, if the 
patient survives long enough, to excavation. 

Chronic Ulcerative Tuberculosis. — In advanced cases the lesions 
are quite diversified, consisting of gray and yellow tubercles, foci of 
bronchopneumonia, diffuse tuberculous infiltration with caseation, 
excavations, fibrous changes in the lung and pleura, etc. The disease 
begins with the development of gray tubercles, most commonly in 
the apex of the upper lobe (most frequently the right), about an inch 
to an inch and a half below the extreme limit of the lung; that is, about 
the distribution of the posterior apical bronchus. This has been attrib- 
uted to inefficient expansion of this region owing to the proximity of the 
clavicle and to a relatively poor blood supply. The process may also 
begin in the apex of the lower lobe (about an inch below its uppermost 
limit, corresponding to the fifth thoracic vertebral spine). Wherever the 
tubercles first develop, they tend to progress downward; but in some 
cases the primary lesions are low down, at the base of one or the other 
lung. When advanced there may be few or many tubercles — of both the 
gray and the yellow variety; and they may be confined to a small section 
of one lobe, or they may be scattered throughout an entire lung or both 
lungs. In cases of rather rapid course, about a more or less obviously 
primary focus there maybe many young tubercles, with comparatively little 
caseation: the patient has been overwhelmed by the toxemia. In more 
chronic cases conglomerate tubercles form, and eventually undergoing 
caseation and softening and leading to ulceration of the wall of a bronchus, 
discharge their softened contents externally; a so-called cavity results. 



110 BACTERIAL INFECTIONS 

These cavities are most common in or near the apex (the seat of the oldest 
lesions); they vary much in size and in number, and they are usually 
surrounded by more or less fibrosis, which surrounds also the adjacent 
bronchi. These destructive changes are commonly due to the associa- 
tion of pyogenic cocci with the tubercle bacilli; that is, they are evidences 
of mixed infection. In some cases there is more or less fibrosis aside 
from that about cavities ; this fibrosis may partly or completely enclose a 
tuberculous focus, isolating it from the remainder of the lung; in other 
cases strands of fibrous tissue pervade and may ultimately replace the 
tuberculous focus — the process has become healed. 

Chronic Fibroid Tuberculosis. — In addition to the aforementioned 
fibrosis about a tuberculous focus, more or less extensive fibrosis may 
occur concurrently with an active tuberculosis — of the chronic ulcerative 
or chronic bronchopneumonic type; or it may occur in association with 
chronic pleural adhesions. The fibrosis may be so extensive as almost 
if not quite completely to replace the pulmonary tissue of an entire lobe 
or more; there may be cavity formation; and there is usually dilatation 
of the smaller and medium-sized bronchi (bronchiectasis). In all cases 
of tuberculosis of the lung, of whatever variety, pleural adhesions are the 
rule ; empyema is quite common ; and from rupture of a tuberculous cavity 
into the pleura pyopneumothorax may develop. 

Symptoms. — Acute Pneumonic Tuberculosis. — In the adult the 
onset is often quite like that of ordinary croupous pneumonia; the physi- 
cal signs are those of solidification of a lobe or an entire lung; and the 
course of the disorder is not notably different from that commonly seen 
in pneumococcic infection of the lung. Suspicion of the real nature of the 
disorder commonly is not entertained until the expected crisis fails to 
occur. The tuberculous nature of the infection, however, is sometimes 
suggested by antecedent ill health of the patient, an ill-explained cough 
lasting for several months, a more or less well-defined tuberculous lesion 
in the lung, bloody rather than rusty sputum, sweating, emaciation, 
remittent rather than continuous fever, slight leukocytosis, and later the 
detection of tubercle bacilli in the sputum. The bronchopneumonic 
type sometimes develops in a person previously well, but it is most 
likely to occur in subjects in general ill health, or in children after measles, 
pertussis, and other infections. The symptoms and physical signs, in 
the beginning at least, are quite like those of bronchopneumonia develop- 
ing under other circumstances and due to other microorganisms; but at the 
end of ten days or two weeks the patient, especially if a child, seems to 
fail markedly in general health, to become emaciated, to develop chills, 
sweats, and hectic fever, and, if he does not die soon, gradually presents 
the common manifestations of chronic ulcerative tuberculosis. 

Chronic Ulcerative Tuberculosis. — This, the common type of 
tuberculosis of the lungs, may reveal itself at the onset in a variety of 
ways. The first symptoms may be those of general ill health, with loss 
of appetite and of weight, without localizing symptoms; or those of 
anemia, especially common in young girls, and usually mistaken for 



TUBERCULOSIS OF THE RESPIRATORY SYSTEM 111 

chlorosis; or those of bronchitis (a "cold" that does not get well), 
laryngitis, pleuritis, hemoptysis, fistula in ano, etc. 

The classical symptom of pulmonary tuberculosis is cough, although 
in a few cases it is absent until an advanced stage of the disease. In 
many cases it is the first symptom that calls attention to the pulmonary 
condition. It may be severe and very harassing to the patient, but, on 
the contrary, it is often mild and disturbs the patient only upon arising 
in the morning. In the beginning the cough is dry, but as bronchial 
irritation increases and disintegration of the pulmonary tissues develops, 
sputum appears. At first this is mucoid in character, but when second- 
ary infection by pyococci takes place it becomes mucopurulent. In an 
advanced stage, the sputum often contains small, hard, coin-like masses, 
by which it is designated as "nummular" in character. Elastic tissue 
evidencing the destruction of the lung is often found, not only in these 
masses, but also free in the sputum. Except in the earliest stage tubercle 
bacilli also are found; to these late in the disease other microorganisms are 
added, chiefly staphylococci, streptococci, pneumococci, and Micrococcus 
tetragenus. Early in the disease the sputum usually contains more or 
less bronchial and alveolar epithelium, the latter having been held at 
one time to be diagnostic of the disease. When a mixed infection is 
present pus cells are found. 

Hemoptysis not infrequently is the first manifestation. Usually only 
a moderate amount of blood is lost, and this is ascribed to pulmonary 
congestion. In some cases small, frequently repeated hemoptyses 
occur during the course of the disease, and for several days following 
such manifestations the sputum is blood-streaked. Later in such cases 
larger hemoptyses may ensue, but they rarely lead directly to death. 
In the latter stages the blood is derived from eroded bloodvessels adja- 
cent to or within cavities. There is a surprisingly large number of cases 
in which no hemorrhage occurs at any time, not even when large cavities 
are present. 

Loss of weight is an important early sign, and in many instances 
precedes the development of cough, expectoration, and hemoptysis. 
If it be associated with a slight rise of temperature in the afternoon 
or early evening, suspicions should be immediately aroused as to its 
tuberculous basis. The association of these two symptoms is of vital 
importance in the diagnosis of the disease. In the very earliest stage 
the temperature may be subnormal; but usually when the patient 
comes under observation, there is a little fever, amounting usually to 
1° or 1.5° F., and the temperature is likely to be very unstable. As 
the disease advances the temperature increases, so that finally it becomes 
typically hectic in character, the morning temperature being subnormal 
and the afternoon temperature (3 to 6 p.m. or thereabout) reaching 
103° to 104° F. (Fig. 3). The highest temperatures are seen in acute 
pulmonary involvement; the development of an acute pneumonic process 
in the chronic form of tuberculosis adds materially to the temperature. 
The fever is referable to the toxemia. The pulse rate is also increased, 



112 



BACTERIAL INFECTIONS 



even in an early stage; later it is usually increased proportionately with 
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development of cavities, the dyspnoea may become marked. This, how- 
ever, is not always dependent upon the amount of lung involvement, 
since in early cases there may be marked dyspnoea, due doubtless to a 
toxic influence on the respiratory centre. On the contrary, in some 
advanced cases there is remarkably little dyspnoea. 

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Intermitting, hectic fever in pulmonary tuberculosis. (Musser.) 



Practically all patients complain at one time or another of thoracic 
pains. In many these develop early, and they may be unilateral or 
bilateral in distribution. They may be a symptom of pleurisy or inter- 
costal neuralgia, and do not necessarily appear upon the same side of the 
chest as the lesion. Sometimes the pains are out of all proportion to the 
extent of pulmonary or pleural involvement. They are sharp or stitch- 
like in character and are intensified usually by deep breathing and cough- 
ing. They may be felt in any part of the chest, but the points of predi- 
lection are about the nipples, in the axillae, and near the angles of the 
scapula?. Tendreness of the thorax is not an infrequent symptom, and 
it seems to be independent of pleuritic conditions. However, many cases 
show tenderness over the pulmonary lesion. The overlying intercostal 
muscles may be quite rigid and contracted. 

Night sweats are characteristic, especially in the advanced stage of the 
chronic form and throughout the course of the acute form. The sweats 
may be moderate or severe, the latter being more frequently seen 
in the acute type of the disease. They are probably the result of a 
depressant action of mixed toxins (tuberculous and pyococcic) upon 
the vasomotor system. 

Loss of appetite may be noted early; but in some cases the patients do 



TUBERCULOSIS OF THE RESPIRATORY SYSTEM 113 

not present this symptom until the disease is far advanced. Vomiting 
is a distressing symptom manifested in some cases and has no connection 
apparently with gastric disease, but rather with the cough. It is seen 
more frequently in the morning than at any other time of the day, and is 
induced by severe attacks of coughing which not infrequently follow 
breakfast. It usually attends cavity formation. There is no constant 
symptom referable to the intestinal tract, though the majority of patients 
are constipated. If a persistent diarrhoea is present, tuberculosis of the 
intestines may be suspected. Often the stools give evidence of deficient 
biliary secretion. From time to time the patient complains of abdominal 
pains, which are often referable to constipation and biliousness. As the 
disease advances some subjects show a decreased elimination of urine 
owing to nephritis, which is likely to develop sooner or later. Hoarse- 
ness not infrequently appears in the bedridden patient in consequence 
of a terminal laryngeal infection; in a few cases the distressing symptoms 
of laryngitis develop at an earlier period. From time to time, even from 
the earliest stage of the disease, headache is complained of, and is due 
doubtless to the toxic condition of the brain centres or to defective 
excretion, or both. Coincidently with the development of these symptoms 
the patient gradually loses in strength and weight; in the very chronic 
cases extreme emaciation is seen, and is associated with a hectic flush 
of the cheeks, hollow, staring eyes, etc. 

In those patients in whom tuberculosis has assumed a very chronic 
form incurvation of the nails and clubbing of the fingers and sometimes 
of the toes develop. These require considerable time for their develop- 
ment, and are probably dependent upon a toxic influence and peripheral 
passive congestion. Such extremities are always cyanosed and cold, as 
a result of defective circulation. 

Physical Signs. — In advanced cases the disease may be disclosed 
by a long, narrow, and flat chest, with an acute epigastric angle, and 
protruding scapulae (alar or winged chest). In many cases, however, 
these signs are absent for a long time. The earliest physical signs con- 
sist of deficient expansion, lagging behind or depression, of one apex 
(usually the right) anteriorly or posteriorly; increased tactile and vocal 
fremitus; impaired percussion resonance (sometimes for a time masked 
by compensatory inflation or emphysema of the surrounding portion 
of the lung, which then yields a vesiculotympanitic note) ; and weak or 
harsh, vesicular breath sounds with prolongation of the expiration. In 
the early stages it is often difficult to determine whether these signs are 
more pronounced that the normal differences between the two apices. 
Soon, however, fine crackling and perhaps fine bubbling rales become 
apparent; and the breath sounds may take on the so-called cogwheel 
character (which occurs also in other conditions). As the disease ad- 
vances (the infiltration of the lung increases) these signs become more 
marked and extend over a wider area, and very commonly they develop 
at the other apex, or in the apex of one of the lower lobes. The percussion 
note becomes actually dull, and tactile and vocal fremitus much exag- 



114 BACTERIAL INFECTIONS 

gerated, the breath sounds bronchovesicular or bronchial, the rales much 
more numerous, and to those previously present coarser bubbling 
(bronchitic) rales are added. Pleural frictions also are frequently 
audible, but it is often almost impossible to distinguish them from 
rales, especially when rales are numerous. Over an area of excavation 
(cavity formation) the tactile and vocal fremitus may be much increased 
unless the overlying pleura is much thickened; bronchophony and pecto- 
riloquy are likely to be elicited; the percussion note is vesiculotympanitic 
or distinctly tympanitic, and the so-called cracked-pot sound may be 
elicited, if the cavity is near the surface, is of fair size (about two inches 
or more in diameter), has thin resilient walls, and communicates with an 
open bronchus. The occurrence of tympany over a previously dull area 
following the evacuation of considerable sputum is quite significant of a 
cavity, but other changes in the percussion note may occur, although they 
are inconstant and of minor diagnostic importance : such as, variations 
in the note, depending upon whether the patient is in the upright or the 
recumbent position (Gerhardt's sign), which occurs over cavities of 
unequal axes, partly filled with fluid, and communicating with an open 
bronchus; a louder and higher pitched tympanitic note when the patient's 
mouth is open as contrasted with the note elicited when the mouth is 
closed (Wintrich's sign); inspiratory increase and expiratory decrease in 
the loudness and pitch of the note (Friedreich's sign); the breath sounds 
become bronchial, cavernous, or amphoric in character; and coarse 
bubbling or gurgling, sometimes resonant, rales may be heard. Myotatic 
irritability (myoidcema) is quite common in advanced cases. Over the 
diseased area the intercostal muscles may be rigid; and there may be local 
tenderness, due sometimes to localized pleuritis, sometimes perhaps 
to toxic influences on the nerves. Percussion over an area of excavation, 
especially in the subclavicular region, may lead to immediate cough and 
expectoration (Erni's tapotage sign). A systolic murmur is often audi- 
ble over the subclavian artery, and is referable to pleural adhesions, 
compressing or distorting the artery. Early in the course of the disease 
the heart usually reveals no abnormality, aside from accentuation of the 
pulmonary second sound, the result of congestion of the lungs; later a 
functional systolic murmur commonly develops, and a systolic murmur of 
relative mitral insufficiency— from dilatation; and the area of cardiac 
dulness may become increased — which, however, is due to retraction of 
the borders of the lungs (especially the left) rather than to enlargement 
of the heart. Cardiopulmonary murmurs also are common. The liver 
and perhaps the spleen may be enlarged— the liver from fatty infiltration; 
both organs from tuberculosis or amyloid disease. 

Chronic Fibroid Tuberculosis.— The chief symptoms consist of 
cough, mucopurulent expectoration, and dyspnoea; the sputum may be 
fei id in the event of bronchiectasis— which is common. Recurring attacks 
of hemoptysis are rather frequent: I have seen a subject in whom these 
occurred over a period of more than twenty years, with maintenance 
of good general health, the weight being about or nearly two hundred 



TUBERCULOSIS OF THE RESPIRATORY SYSTEM 115 

pounds. From time to time there may be attacks of more or less fever. 
The physical signs are those of chronic interstitial pneumonitis: distor- 
tion and insinking of the chest, with uncovering and perhaps displace- 
ment of the heart; and over the affected area dulness on percussion, in- 
creased tactile and vocal fremitus (except in the event of pleural adhesions 
which are rather common), bronchovesicular or bronchial breath sounds, 
and fine or coarse bubbling rales. 

Diagnosis. — Acute pneumonic tuberculosis, since it resembles ordinary 
croupous pneumonia in its mode of onset and its course, is commonly 
not recognized until the expected crisis does not occur; but certain of 
the aberrant phenomena already mentioned may excite suspicion of the 
tuberculous nature of the infection and sometimes lead the observing 
physician to an early diagnosis. Chronic ulcerative tuberculosis is dis- 
closed by any of the aforementioned early symptoms, especially slight 
or progressive loss of weight; early subnormal temperature, but rather 
soon slight afternoon fever; rapid and unstable pulse; cough with or 
without slight expectoration; even slight hemoptysis; and the physical 
signs of beginning infiltration of the lung — usually one apex. One should 
endeavor to make the diagnosis before tubercle bacilli appear in the 
sputum; their detection as well as the presence of elastic fibers makes 
the diagnosis conclusive. In the event of doubt recourse may be had to 
one of the several tuberculin tests (page 125). Radiographic examination 
often enables one to detect a tuberculous focus in the lung otherwise 
insusceptible of recognition. In the differential diagnosis one must 
exclude syphilis, actinomycosis, streptothricosis, and malignant disease 
of the lungs. Syphilis of the lung is rare, and the diagnosis can seldom 
be made with certainty; the disorder may be suspected upon the develop- 
ment in a known syphilitic subject of the physical signs of chronic inter- 
stitial pneumonitis, with perhaps bronchiectasis of the lower lobe, and 
the absence from the sputum of tubercle bacilli; but one must remember 
that tuberculosis of the lungs may occur in a syphilitic subject and that 
tubercle bacilli may not be found for some time; a positive Wassermann 
reaction may be of some assistance. Actinomycosis and streptothrical 
infections are recognizable by the detection in the sputum of the specific 
infectious agent. In malignant disease there is usually little if any fever; 
the physical signs are those of irregular solidification — in one, sometimes 
in both, lungs; secondary anemia and cachexia soon supervene; the spu- 
tum is often blood-tinged or it may be distinctly bloody, and may reveal 
tumor cells, but no tubercle bacilli. Chronic fibroid tuberculosis is 
readily recognized by the physical signs of chronic interstitial pneu- 
monitis and the presence of tubercle bacilli in the sputum. 

Prognosis. — Acute pneumonic tuberculosis usually leads to death in 
from four to eight weeks; rarely the progress of the disorder becomes 
somewhat stayed, and the process may become chronic, but a fatal 
termination seems inevitable. Death in some of the chronic forms of 
pulmonary tuberculosis may be finally induced by the acute pneumonic 
or bronchopneumonic process. In chronic ulcerative tuberculosis the 



116 BACTERIAL INFECTIONS 

prognosis depends upon the extent of the process when detected, the 
resistance of the individual, his occupation and other social environment, 
the ability or lack of ability to place himself under the best hygienic, 
medical, and other conditions, etc. A poor general condition, poverty, 
inappropriate and insufficient food, exhausting work, mental cares and 
anxiety, etc., are potent deterrents of recovery. In incipient and even 
moderately advanced cases, under favorable circumstances and the best 
hygienic surroundings, the outlook is good, if not for recovery, at least 
for comparative comfort and prolongation of life. Chronic fibroid 
tuberculosis may be a fortunate outcome of the chronic ulcerative process, 
but whether developing thus or otherwise, it may last for many (twenty 
or more) years. 

Classification. — The American Sanatorium Association, approving a 
committee report, suggests the use of the following classification of 
patients upon admission and discharge and for ultimate results; the 
classification is equally applicable in private practice : 

1. On Admission. — These definitions indicate the furthest extent 
of the disease and the greatest severity of symptoms that a patient can 
present and still belong to the stage defined. All patients beyond the 
incipient stage fall under the moderately advanced stage unless the 
physical signs and symptoms exceed those of the moderately advanced 
stage, when they should be classified as far advanced. 

Incipient. — Slight or no constitutional symptoms (including particu- 
larly gastric or intestinal disturbance or rapid loss of weight); slight or 
no elevation of temperature or acceleration of pulse at any time during 
the twenty-four hours. Expectoration usually small in amount or 
absent; tubercle bacilli may be present or absent. Slight infiltration 
limited to the apex of one or both lungs or a small part of one lung. No 
tuberculous complications. 

Moderately Advanced. — No marked impairment of function, either 
local or constitutional. Localized consolidation, moderate in extent with 
little or no evidence of cavity formation; or infiltration more extensive 
than under incipient. No serious complications. 

Far Advanced. — Marked impairment of function, local and constitu- 
tional. Marked consolidation of an entire lobe; or disseminated areas 
of beginning cavity formation; or serious complications. 

.1 / ilia ry Tuberculosis. 

'2. On Discharge.— Apparently Cured. — All constitutional symp- 
toms and expectoration with bacilli absent for a period of three months 
and the physical signs to be those of a healed lesion. 

Arrested. Absence of all constitutional symptoms; expectoration 
and bacilli may or may not be present; physical signs stationary or 
retrogressive; the foregoing conditions to have existed for at least two 
months | a somewhat arbitrary period, intended to cover the cases, which 
Frequently occur, of patients who leave the sanatorium for various 
reasons, contrary to advice, after a stay of a few weeks, although all 
active symptoms may have ceased completely soon after entrance). 



TUBERCULOSIS OF THE DIGESTIVE SYSTEM 117 

Improved. — Constitutional symptoms lessened or entirely absent; 
physical signs improved or unchanged; cough and expectoration with 
bacilli usually present. 

Unimproved or Progressive. — All essential symptoms and signs un- 
abated or increased. 

Died. 

3. Ultimate Results. — Cured. — All constitutional symptoms and 
expectoration with bacilli absent for a period of two years under ordi- 
nary conditions of life. 

Well. — Patients who fulfil all the conditions required under "cured," 
but about whose sputum no definite information can be obtained. 

Arrested, Improved, Progressive. — As above. 

Dead. 

Tuberculosis of the Digestive System. 

Mouth. — Tuberculous ulceration of the mouth and tongue is rare, and 
is usually secondary to laryngeal or pulmonary involvement. The affec- 
tion simulates syphilitic and malignant ulceration. The tuberculous 
lesion is commonly solitary, sharply outlined, and pale in color, with 
an area of cedematous tissue often surrounding it. It is superficially 
located, at least in its early stage. The syphilitic lesion is generally an 
ulcerated gumma, and is deeply placed. The malignant (carcinomatous) 
ulcer occurs usually later in life, and considerable induration usually 
appears about its margin. A tuberculin test may serve to dispel any 
doubt in regard to the diagnosis, foi the ulcerated tissue is likely to show 
some reaction if tuberculosis is present. 

Tonsils and Pharynx. — Tuberculosis of the tonsils may be pri- 
mary or secondary. It is not improbable that infection finds its way into 
the system in many cases through these tissues. However, it seems 
likely that the majority of cases are secondary and are induced by sputum 
from an infected lung. The disease appears as caseous foci adjacent 
to the crypts, and is very common in the advanced stage of pulmonary 
tuberculosis. The pharynx is even less frequently the seat of tubercu- 
losis than is the oral mucous membrane. The miliary type is the 
commonest, and this by progress or confluence of the lesions may give 
rise to ulceration, which may occur in advanced pulmonary tuberculosis. 

(Esophagus. — The oesophagus is rarely the seat of tuberculosis. 
Occasionally caseous bronchial and tracheal lymph nodes erode through 
the oesophageal wall and cause ulceration therein. More rarely the 
lesion develops in consequence of an abrasion of the mucosa; this has 
been noted in a few cases of malignant ulceration, in which tubercles 
have been noted in the wall. 

Stomach. — Aside from the development of tuberculous masses 
in the peritoneal tissues of the gastric wall coincidently with tuberculous 
peritonitis, tuberculosis of the stomach is very rare. The usual mani- 
festation is ulceration of the mucous membrane, which is somewhat 
more frequently found in infancy and childhood than in later life. The 



118 BACTERIAL INFECTIONS 

lesions may be solitary or multiple, commonly the latter, and they are 
superficially placed. In a few cases tuberculosis has been known to 
become engrafted upon a previously existing simple ulcer. There are 
no specific symptoms. It may be associated with intestinal ulceration. 

Intestines. — The frequency of involvement of the small intestine 
increases progressively toward the ileocecal valve, since the lymphoid 
tissue is the seat of predilection and this tissue is present in abundance 
in the ileum. The appendix and cecum are also commonly diseased. 
The remainder of the large intestine is affected more frequently than the 
duodenum or jejunum. The immunity of the duodenum to infection 
has been ascribed to the acid intestinal contents and to the rapidity 
of the intestinal current. The source of intestinal infection is chiefly 
infected milk and butter and the swallowing of tuberculous sputum. 
In infancy and childhood the bacilli seem capable of penetrating the walls 
of the intestines without inducing any lesions, and they are then carried 
to the mesenteric nodes, where a focus of disease is set up. Such perme- 
ability of the intestinal mucosa seems not to obtain in adult life. Intes- 
tinal ulceration is noted rather more frequently in the latter period of 
life. Alimentary infection is not the sole source of the disease, for in 
cases of acute generalized miliary tuberculosis the bacilli are carried 
by the blood and give rise to the characteristic tubercles. 

Pathology. — The ulcer is the usual form of intestinal tuberculosis. It 
is probably produced by the coalescence of several adjacent foci and the 
erosion of the mucous surface. The lesion has a ragged, punched-out 
appearance, with an elevated and somewhat indurated margin. Con- 
gestion of the adjacent tissues may or may not be present. Typically 
the ulcer extends along the gut in a circular manner; this has been 
ascribed to the infection following the course of the lymphatics. The 
ulcers vary in size from that of a millet seed to a diameter of four or five 
inches. On the serous surface of the bowel opposite the lesions miliary 
tubercles are commonly found. It is rare to find that an ulcer has 
perforated, such an accident being apparently inhibited by an over- 
growth of the tissues at its base. When perforation occurs adhesions 
develop between the adjacent coils of intestines, indicating a localized 
peritonitis; at times a generalized peritonitis is the consequence. An 
unusual form of intestinal tuberculosis is that in which marked hyper- 
plastic changes take place without notable caseation and ulceration. 
This may be found in any part of the intestine, but there is a predilection 
for the cecal tissues; a certain degree of stenosis may co-exist. A rectal 
or anal fistula may be the result of infection of the lowermost portion 
of the intestinal tract. In cases of pulmonary tuberculosis 4 to 5 per 
cent, show such fistulse, which may be clinically the primary lesion. 

Symptoms. The symptoms are indefinite; some patients have diar- 
rhoea, while others exhibit no symptoms referable to the bowels. Diar- 
rhea with abdominal pains and tenderness in a tuberculous patient is 
always suggestive of intestinal involvement. Involvement of the colon 
seems to be provocative of diarrhoea more frequently than involvement 



TUBERCULOSIS OF THE DIGESTIVE SYSTEM 119 

of the small intestine only. Intestinal infection complicates pulmonary 
tuberculosis in from 60 to 75 per cent, of the cases, especially in adults. 

Diagnosis. — It is practically impossible to differentiate intestinal 
tuberculosis from simple enteritis or enterocolitis. Bloody stools are 
suggestive of ulceration. If the diarrhoea is refractory to medication, 
the condition is likely to be tuberculous in character. The finding of 
tubercle bacilli in the feces is not necessarily diagnostic. In children 
the diagnosis is made with even greater difficulty than in adults. If a 
fistula is present the feces may show traces of pus. 

Prognosis. — The prognosis is unfavorable, although in some cases 
cicatrization and healing of the ulcers ensues. Doubtless the condition 
hastens a fatal issue, on account of the deterioration of the intestinal 
functions and the increased toxemia promoted by a large ulcerated and 
infected surface. 

Liver. — Tuberculosis of the liver develops mainly as a result of infec- 
tion through the hepatic artery and the portal vein; it is possible that 
some cases are referable to the entrance of infectious material through 
the lymphatics from the gastrohepatic nodes and through the biliary 
channels. The commonest sources of infection are the lungs and 
the intestines, coincidently with the development of acute generalized 
miliary tuberculosis. The commonest type of hepatic involvement 
is the miliary, in which the characteristic tubercles are seen, not only in 
the parenchyma of the organ, but frequently upon its peritoneal surface. 
The organ is likely to be moderately enlarged. Another type is that in 
which large caseous masses appear; these sometimes soften and give 
rise to abscesses and cavities. The condition is very rare. A ques- 
tionable type, tuberculous cirrhosis, has been described in which there 
are no lesions except hyperplastic changes in the connective tissue. 
There are no characteristic symptoms, except occasional jaundice, in 
miliary and caseous tuberculosis of the liver, but upon examination the 
organ may be found moderately enlarged. In chronic suppurative 
tuberculosis elsewhere in the body (bones, etc.), amyloid disease may co- 
exist and the organ may be considerably enlarged. In a few of the 
rare cases of tuberculous abscess the mass protrudes from the costal 
margin. 

Pancreas. — Tuberculosis of the pancreas resembles that of the liver, 
since the miliary type is the commonest, though the organ is much less 
frequently involved than the liver. It has been stated that this condition 
is a pathological curiosity and that involvement of the pancreas is one 
of the rarest manifestations of tuberculosis. A more thorough study in 
recent years reveals the fact that the organ is not uncommonly affected, 
and in children as many as 44 per cent, of cases of generalized disease 
have been found to show tuberculous pancreatitis. In adult life the 
condition is much less frequently seen. Cases of primary involvement 
have been described, but these lack substantial proof. It is probable 
that every case is secondary to some other focus in the body, and that in a 
preponderance of these cases infection reaches the organ by way of the 



120 BACTERIAL INFECTIONS 

blood channels, that is, coincidently with a generalized miliary disease. 
There are two other possible methods of entrance of infection — by 
the lymphatics and by the pancreatic ducts. A few cases have been 
reported in which large caseous foci were found in the parenchyma of 
the organ, and in which there was associated involvement of the 
adjacent lymph nodes. It is likely that in some of these instances the 
true condition was enlargement and caseation of the nodes, with encroach- 
ment upon but no direct involvement of the pancreas. No authentic 
cases have been described in which infection took place through the 
ducts from the intestines. There are no symptoms indicative of pan- 
creatic tuberculosis. 

Tuberculosis of the Genito-urinary System. 

Male Genitalia. — Tuberculosis of the testicle is not uncommon 
between the ages of twenty and forty years. In the majority of cases, 
the process is secondary to a focus elsewhere (hemogenic infection), or 
it follows tuberculosis of some other portion of the genito-urinary system 
(infection occurring along the vas deferens). The progess is usually 
unilateral, though it may be bilateral. It develops in an insidious manner 
in the epididymis as a small firm mass; later the body of the testicle may 
become invaded, and the lesions undergoing caseation and softening- 
may form a connection with the overlying skin and discharge externally, 
leaving sinuses ; or the process may extend along the vas deferens, infect- 
ing it, and later involving the seminal vesicles, the prostate, the bladder, 
the ureters, the kidneys, etc. The semen being infected may lead to 
tuberculosis of the female genitalia. 

Female Genitalia.— The Fallopian tube is more frequently tuber- 
culous than any other part of the female generative system. It has been 
stated that from 8 to 16 per cent, of specimens removed at operation for 
inflammatory disease are found to be tuberculous. The source of 
infection may be the blood, the peritoneum, or the lower genital tract. 
The disease is primarily one of tubercle formation within the mucosa; 
this eventually gives rise to nodular, caseous masses and general destruc- 
tion of the tubal and oftentimes of the ovarian tissues. In many cases 
of tuberculous peritonitis the tubes are the nidus from which infection is 
disseminated. There are no specific symptoms aside from those com- 
mon to ordinary tuboovarian disease. The uterus may present evi- 
dences of tuberculosis primarily, as miliary tubercles in the endometrium; 
after a time large cheesy masses may appear. Infection may occur from 
the tubes, vagina, or from the circulating blood; tuberculous semen may 
be responsible for some cases. The disease has been diagnosticated by 
curettage and the removal of particles of the endometrium in which 
tubercles and bacilli have been found. 

The mammary (/lands are rarely the seat of tuberculosis. The sources 
of infection are adjacent lymphatic and osseous lesions. Primarily 
the condition is one of miliary tuberculosis, followed by the production 



TUBERCULOSIS OF THE GENITO-URINARY SYSTEM 121 

of caseous foci, from which sinuses develop to the cutaneous surface. 
Multiple areas of ulceration are not infrequently seen. The diagnosis 
is confirmed by histological examination of tissues or by finding tubercle 
bacilli in the purulent material. 

Urinary System. — Renal tuberculosis is present in from 40 to 50 
per cent, of cases of pulmonary infection. Recent studies have shown 
that the condition is much commoner than was formerly considered. 
The infection may be hemogenic, lymphogenic, or urogenic. The com- 
monest type is miliary tuberculosis, which is induced by blood infec- 
tion, as it is in all other organs of the body. The lesions are bilateral; 
the cortex especially shows the presence of the characteristic tubercles, 
associated with which there is usually moderate hyperplasia of the 
interstitial tissues. Disease of the retroperitoneal nodes may extend 
to the kidney (lymphogenic infection), in which event the condition is 
generally unilateral. One rather large caseous focus may mark the 
disease. These two types have no special symptomatology; the detection 
of tubercle bacilli in the urine, though of great importance, may not 
necessarily signify renal tuberculosis, since it has been stated that tubercle 
bacilli may be excreted by tuberculous subjects in whom the kidneys 
appear to be unaffected. Some of the supposed tubercle bacilli, however, 
are doubtless smegma or other acid-fast organisms. The kidneys may 
become diseased as the result of an infection from the bladder through 
the ureters (urogenous infection), the ureters often showing no evidences 
of tuberculosis. Commonly the infection passes first up one ureter and 
then after a variable period up the other. Gonorrhoea has been sug- 
gested as a predisposing cause. The renal pelvis and calyces are first 
affected; thence the medullary and cortical parts are attacked. Often 
there is considerable dilatation of the pelvis, in consequence of more or 
less stenosis of the ureter. The condition is slowly progressive, caseation 
and widespread destruction of the tissues occurring, so that usually the 
kidney after a time assumes a multiloculated appearance. The walls 
of the cavities are rough, ragged, and necrotic, and it is not unusual to 
find the parenchymatous tissue completely destroyed, and the organ con- 
siderably enlarged (pyonephrosis). Hematuria, pyuria, and bacilluria 
are symptoms. Upon examination the enlarged organ or organs may be 
well outlined, and a certain amount of tenderness may be elicited over the 
lumbar region. The condition is to be differentiated from malignant 
disease of the kidney. The bladder may be the seat of tuberculosis; 
infection may occur through the urethra by means of infected instru- 
ments or coincidently with gonorrhoea, or by way of the blood stream; or 
in consequence of kidney involvement; or from the reproductive organs 
of the male sex. As a consequence the vesical wall becomes invaded 
by tubercles, caseous masses, or it becomes ulcerated. The symptoms 
are those of cystitis, together with pyuria and bacilluria. The urethra is 
rarely the seat of tuberculosis. The predisposing factors are gonorrhoea, 
stricture, and phimosis. Infection may occur from the use of infected 
instruments or, especially in the female, it may follow tuberculosis of 



122 BACTERIAL INFECTIONS 

the lower genital tract; the condition is much less likely due to a descend- 
ing infection. 

Tuberculosis of the Nervous System. 

Brain. — Tuberculosis of the cerebral meninges is associated with 
generalized miliary disease in about 75 per cent, of the cases, and the 
infection, therefore, is chiefly hemogenic in type. The disorder is 
most frequently seen in childhood, especially prior to the sixth year. 
Meningeal infection is not an infrequent complication of tuberculosis 
of the reproductive and osseous system; moreover, it has been shown that 
it may be a sequel of operations for the relief of bone and joint disease, 
and that it is not infrequently a sequel of measles and whooping cough, 
in which it is probable that the primary lesion is present in the cervical 
or bronchial lymph nodes. On the contrary, meningeal disease may 
arise in consequence of lymphatic dissemination, or by direct continuity of 
structure. Tuberculosis of the eye, ear, and cervical nodes may set up 
the condition. A few cases have been reported in which the infection 
occurred through the cribriform plate of the ethmoid bone from a tuber- 
culous rhinitis. Primary cases of meningeal tuberculosis are of doubtful 
existence. 

Pathology. — The disease usually appears as a leptomeningitis, but in 
some instances it is a true meningo-encephalitis. The base is more 
commonly affected than the convexity. There are two chief types of the 
disease : one in which miliary tubercles are found, and the other in which 
large caseous nodules (so-called solitary tubercles) are encountered. The 
condition may be localized or diffused throughout the meningeal surfaces. 
The miliary tubercles may be scattered over the serous membranes; 
with these there is always more or less exudate present, which serves 
to flatten the convolutions. The lateral ventricles are usually found to 
contain an excess of fluid, and this, likewise, may be seen in the third and 
fourth ventricles, the condition being known as internal hydrocephalus. 
In the other type one or more large caseous nodules are present, usually 
over the basal portions of the brain. An excess of fluid in the ventricles 
usually co-exists. Occasionally chronic leptomeningitis is manifested by 
thickening of the membranes, and is associated with the presence of a 
few small caseous masses, the condition being indicative apparently of a 
healing process. Similar lesions may be found in the spinal cord and 
its meninges. 

Symptoms. — When meningitis supervenes in a case of acute generalized 
miliary tuberculosis, its attending symptoms overshadow all those pre- 
viously existing. The onset may be insidious or abrupt, usually the 
former. There may be a period of vague prodromes during which 
languor, irritability, headache, vomiting, and constipation may appear. 
I difficulties in speech are sometimes noted early in the condition. After 
a time certain characteristic symptoms appear, so that the disease may 
livided into three stages: (1) the stage of irritation which is referable 



>e (l 



TUBERCULOSIS OF THE NERVOUS SYSTEM 123 

to the meninges and cortex; (2) the stage of pressure, referable to the 
effusion into the ventricles; (3) the stage of paralysis, referable to in- 
creased pressure and extension of the disease to the medulla oblongata. 
The symptoms of the first and second stages usually overlap. In the 
early stage the face is commonly flushed, and by stroking the skin 
upon any part of the body the tache cerebrale is usually obtained. The 
pupils are dilated and photophobia may be marked, especially in adults. 
Headache is a common symptom, though more frequently noted in 
adults than in children, and it is likely to be frontal in the former and 
generalized in the latter. Pains may be complained of in various parts 
of the body, as in the abdomen, spine, knees, etc., and these joint exacer- 
bations may be so severe that acute rheumatism may be simulated. The 
decubitus is characteristic, the patient lying upon one side with the legs 
drawn up, and he resents any disturbance. Incessant vomiting may be 
present; this is of the cerebral type, sudden, projectile in character, 
unattended by nausea, and occurs independently of taking food. Con- 
stipation is a common symptom usually relieved by aperients, but in 
some instances there seems to be almost complete paralysis of the bowel. 
Diarrhoea may be a symptom; this is likely to be present if intestinal 
tuberculosis is a complication. The temperature is usually not very 
high, but irregular in the early stage, while in the paralytic stage it may 
reach as high as 108° F. The pulse is likely to be slow and irregular 
in the early stage, but later it becomes quickened. In the early stage 
deep, slow respirations are observed, to be followed later by those of 
the Cheyne-Stokes type. Retraction of the head and stiffness of the 
neck are usually not marked, and in many instances they are absent. 
To a great extent these symptoms depend upon involvement of the 
posterior basal portions of the brain. Convulsions may appear in any 
one or all of the stages of tuberculous meningitis; those of the second 
stage are most distinctive, inasmuch as they may serve to determine 
the locality of the inflammation. Paralysis, coma, and death may 
terminate the condition. The symptoms of the solitary tubercle are 
those of brain tumor. 

Diagnosis. — Among the diseases which may simulate tuberculous 
meningitis are typhoid fever, pneumonia, brain tumor, brain abscess, 
and thrombosis of the cerebral sinuses. The probability of confusion 
is greatest in the early stage of the disease, for as it progresses distinctive 
symptoms appear. The temperature is typically lower in meningitis 
than in typhoid fever, and the irritability is greater. In the former, the 
abdomen is retracted, while in the latter it is distended and tympanitic. 
A rather rigid position and a lateral decubitus are seen in meningitis, 
and a relaxed position and a dorsal decubitus are common to typhoid 
fever. The Widal reaction and the results of a study of fluid removed 
by lumbar puncture should eliminate any doubt. The temperature, 
decubitus, and abdominal condition in pneumonia more closely resemble 
typhoid fever than meningitis. In brain tumor the condition is pro- 
longed and the gradual paralysis is very different from that of meningitis; 



124 BACTERIAL INFECTIONS 

optic neuritis is likely to be much more marked than in meningitis. 
Exacerbations of temperature and rigors are characteristic of cerebral 
abscess; these are absent in tuberculous meningitis, at least in its early 
stage. Localized venous engorgement about the eyes and temples and 
the presence of hemorrhage in the fundus of the eye may serve in some 
cases to differentiate thrombosis of the cerebral sinuses from menin- 
geal tuberculosis. 

Prognosis. — The prognosis depends somewhat upon the extent of the 
inflammation, since if it is localized, recovery may possibly occur, but 
as the condition is usually generalized, the disease is looked upon as fatal. 
The course of the average fatal case is from three to four weeks. When 
the disease is generalized over the convexity, the duration is usually 
much shorter than when it has the basal distribution. 

Tuberculosis of the Bones and Joints. 

Tuberculosis of the bones and joints occurs in various forms, such as 
caries of bone, "white swelling," etc. One-half of the cases develop 
prior to the twentieth year; the sexes are affected with equal frequency. 
Traumatism seems to have some predisposing influence; though the 
bacteria do not necessarily enter the system through the channels thus 
induced, the vitality of the part is diminished by reason of the injury. 
Infection gains entrance to the part from a previously existing lesion 
in the majority of instances by the blood stream. In some cases the 
lymph stream cannot be eliminated from consideration. The primary 
focus may be situated in the lungs, genitalia, or lymph nodes. Though 
primary cases of bone and joint tuberculosis have been described, it 
is likely that, at least in the majority of the cases, a latent focus of disease 
was present, probably in a lymph node, as for example in the cervical 
or bronchial groups. So-called primary cases have been observed to 
follow infections such as measles, whooping cough, scarlet fever, etc. 
According to Cornet the disease attacks the bones and joints in the 
following order of frequency : the spinal column, the hip-joint, the small 
joints of the hands and feet, the knee-joint, the long bones, the ankle- 
joint, the tarsus, and the elbow-, shoulder-, and wrist-joints. The 
sternum, ribs, cranial bones, and pelvis are rarely tuberculous. 

Pathology. — Of the bony structures, the cancellous or spongy parts are 
the seats of predilection in the development of tuberculosis; this is seen 
especially in the ends of the long bones and in certain short bones. In 
osseous tuberculosis the epiphysis is the commonest seat of initial in- 
volvement, while in joints the synovial membranes become first infected. 
If the diseased bone is incised longitudinally there is seen, in the early 
stages of the affection, a small, yellowish, nodular mass within the can- 
cellous structure at the epiphysis. Microscopic examination reveals 
numerous tubercles and bacilli. At a later stage of the disease the 
yellowish muss is found to have softened and to contain necrotic particles 
of bone. Still later, if treatment has been effectual, more or less fibrosis 



DIAGNOSIS OF TUBERCULOSIS 125 

of the parts and eburnation of the bone attest the fact that the condition 
is gradually healing. Subsequently much of the fluid is lost and the 
necrotic mass is of a dry, cheesy consistency. On the contrary, gradual 
destruction of the osteal and periosteal tissues may occur ; and the necrotic 
material may be discharged through a sinus or fistula, which has devel- 
oped. At times rupture takes place into the adjacent joint. In many 
cases, however, the joint is primarily affected upon its synovial surfaces. 
The process has the same general character as heretofore described; in 
addition, in the favorable cases extreme fibrosis gives rise to ankylosis 
or stiffening of the joint. 

Symptoms. — The symptoms of bone and joint tuberculosis depend 
somewhat upon the point involved. The condition is typically chronic, 
beginning with vague pains and tenderness, together with gradual 
increase in the size of the part. If a joint is affected, stiffness 
slowly develops. Muscular spasm is often noted rather early in the 
disease; later there is considerable muscular atrophy. The latter condi- 
tion serves to intensify the swollen appearance of the part. The cuta- 
neous tissues are usually pale, and coursing over the part oftentimes 
prominent veins are seen. If treatment is effectual, no further changes 
may be noted, and the condition is likely to heal. If septic infection 
is added to the already existing tuberculous lesions, all the symptoms 
become intensified and the process often goes on to sinus formation, 
the pus from which contains many pyococci, and often but few, if 
any, tubercle bacilli. In spinal caries (Pott's disease), owing to the 
involvement of the bodies of the vertebrae, the process does not tend to 
extend toward the neighboring cutaneous surface, but rather down the 
sheath of the psoas muscle, and appears in the inguinal region. There 
is always more or less spinal deformity in Pott's disease (kyphosis, 
skoliosis). In hip-joint disease there is a tendency toward shortening 
of the affected limb. 

Prognosis. — It is often well to give a guarded prognosis incases of bone 
and joint tuberculosis in so far as the local condition is concerned. 
The possibilities of ankylosis must be kept in mind, for after considerable 
involvement of the structures has taken place complete restoration 
never occurs. Severe cases may give rise to widespread dissemination 
of the infection, and death is the sequel. Amyloid changes characteris- 
tically take place in the viscera (liver, spleen, kidneys, etc.) in conse- 
quence of the chronic tuberculous changes with suppuration. 

General Diagnosis. — In addition to the aforementioned diagnostic 
procedures available in the several types and situations of tuberculosis, 
recourse may be had to tuberculin tests; agglutination tests also have 
been proposed, but they have not proved satisfactory. The tuberculin 
tests comprise: (1) The von Pirquet cutaneous reaction, which consists 
of preliminary scarification and the application to the scarified area of a 
drop of old tuberculin — in a manner analogous to that practised in 
ordinary vaccination; a scarified but otherwise untreated area is used 



126 BACTERIAL INFECTIONS 

as a control. The test is of much value, especially in young subjects; 
in adults the importance of a slight reaction should not be overestimated, 
since many adults are the subject of more or less quiescent tuberculosis, 
of the bronchial lymph nodes, for instance; a marked reaction may be 
significant of reinfection or activation of a quiescent lesion. (2) The 
Moro cutaneous reaction, which consists of rubbing into the skin an 
ointment of old tuberculin and lanolin. The test is of somewhat less 
value than the von Pirquet. (3) The Wolff -Eisner or Calmette con- 
junctival test, which consists in instilling into the conjunctiva of one eye 
one drop of a 0.5 per cent, solution of old tuberculin. The ensuing 
reaction is sometimes so violent that the test deservedly has fallen into 
disrepute and disuse. (4) The hypodermic test, which consists in inject- 
ing 2 milligrams of old tuberculin; the reaction consists in the production, 
within twelve to twenty-four hours, of local irritation, malaise, neuro- 
muscular pains or soreness, and fever (102° to 104°). Should the first in- 
jection prove unproductive, the injections may be increased to 3, 5, and 8 
milligrams. Since the introduction of the von Pirquet test the hypodermic 
test has fallen into disuse. (5) Material (sputum, etc.) from a suspected 
case may be injected into a guinea-pig, and the pig killed at the end of 
four to six weeks (if it has not died earlier). In the event of the material 
having contained tubercle bacilli the animal will be found infected. 
(6) Ebbright has suggested injecting the suspected material into a guinea- 
pig; at the end of six days injecting 0.25 c.c. of old tuberculin; and killing 
the animal at the end of another twenty-four hours. In the event of 
tuberculosis, the bacilli may be found thus early, the view being that the 
large dose of tuberculin breaks down the body resistance and permits the 
rapid multiplication of the tubercle bacilli. (7) Yamamanchi has 
suggested injecting into a rabbit a few cubic centimeters of blood serum 
(or blister serum) from a case of suspected tuberculosis, and in a few 
days injecting tuberculin; the animal having become sensitized, experi- 
ences a severe, perhaps fatal, reaction. (8) The bacilli may be searched 
for in the circulating blood, as suggested by Rosenberger; but they are 
not likely to be found in many cases, assuredly not in early or localized 
infections. 

Prophylaxis. — The control of tuberculosis may eventually be effected 
by prophylactic measures, of which the following are the most important: 
( 1 ) The education of the public, by a continuation of the present-day 
widespread antituberculosis propaganda; by disseminating a knowledge 
of the efficient means of preventing the disease — into municipalities, 
industrial and other associations, schools, the family, etc. (2) Improved 
sanitary conditions under which, especially the poor, the industrial 
workers, etc., live and work. (3) Sanatoriums, hospitals, dispensaries, and 
social services for the study, prevention, and treatment of tuberculosis; 
especially important being the treatment of incipient and far-advanced 
and hopeless eases, and visiting the poor and ill-informed by trained 
nurses or social workers. (4) Supervision by the Public Health authori- 
I ies, winch should include notification of the disease (in a manner to avoid 



TREATMENT OF TUBERCULOSIS 127 

wounding the sensibilities of the patients), the destruction of sputum, 
the disinfecting of rooms inhabited by tuberculous patients, supervision 
of dairies, abattoirs, etc. (5) Individual prophylaxis — which in general 
comprises the regulations laid down on page 29. In addition, children 
of tuberculous parents should have the benefit of the best environmental 
conditions, and assuredly should not sleep in the same rooms with their 
diseased parent or parents. The ideal conditions as regards future health 
suggest rearing the children apart from the tuberculous parent — vir- 
tually impossible of attainment, even were it in every respect desirable 
(which it is not). The child, however, should be out-of-doors as much as 
possible, have an abundance of good nutritious food, be well clad, and 
afforded a sufficiency of regulated exercises. In the event of illness, 
especially catarrhal disorders of the upper respiratory tract, enlarged 
tonsils, adenoids, enlarged cervical lymph nodes, general debility, asthenia 
and anemia, etc., efficient treatment should be instantly undertaken, and 
tonics, such as iron, quinine, strychnine, arsenic, cod-liver oil, etc., 
should be administered. 

Treatment. — The efficient management of tuberculosis in general 
comprises the use of: (1) Fresh air, nutritious food, and regulated rest 
and exercise; (2) specific remedies; (3) medicinal agents, largely to 
combat symptomatic indications; and (4) certain additional measures 
applicable in special forms of tuberculosis, such as miliary tuberculosis, 
acute pneumonic tuberculosis, surgical tuberculosis, etc. 

Fresh Air, Nutritious Food, Rest, and Exercise. — Nothing 
transcends in importance fresh air and nutritious food. The benefits 
of fresh air may be secured at home in the city or the country, in sana- 
toriums near at hand, or in certain mountainous or marine climates. If 
at home, the patient should be as much as possible out-of-doors, and he 
should sleep on a balcony or with the windows of his room wide open; 
he should, of course, be sufficiently, but not excessively clothed (as 
commonly obtains among the ignorant classes), and he should take the 
precaution so to arrange his bed that he is protected against continuous 
draughts, and the rigors of storms. Night air, dampness, rain, snow, and 
the continued low temperature of winter are not contra-indications to 
this open-air treatment; nor are cough, hemoptysis, fever, emaciation, etc. 
Excellent results have been achieved by the tuberculosis classes inau- 
gurated by J. H. Pratt. It is not necessary, as a rule, for the patient to 
go long distances from home to secure the benefits of fresh air; indeed, 
this is positively contra-indicated in advanced cases; in those with strong 
home ties, in whom absence from home often causes marked mental 
depression; and in those to whom such distant travelling occasions 
financial hardships — which are not commensurate with the hoped-for 
advantages. Climate per se is not the major factor in the cure, that 
region being satisfactory that combines a pure atmosphere, considerable 
sunshine, and equable temperature (absence of sudden variations); 
other desirable features comprise dryness of the atmosphere (at least not 
excessive humidity), moderate altitude, and the facilities for good food, 



128 BACTERIAL INFECTIONS 

good housing, and some amusement. Most, especially early, cases, 
with localized lesions, moderate fever, and little emaciation, and without 
excavations, do best at moderate altitudes (2000 to 2500 feet), such as 
the Adirondacks, Asheville, Aiken, etc. These afford the advantage that, 
as a rule, after the disease has been arrested the patient may return to 
the sea level without the likelihood of reactivation of the lesions. Some 
patients seem to do better at higher altitudes (5000 feet or more), such 
as Colorado, New Mexico, Arizona, Davos and other places in Switzer- 
land, etc. Chronic and advanced cases, with excavation, fibrosis, 
emphysema, repeated hemoptysis, emaciation, etc., as a rule, do better 
at the sea level and in a moist climate, such as Florida, Bermuda, etc. 
Subjects with slowly progressing lesions are often much benefited by 
the dryer climate of Southern California, the Riviera, Egypt, Algiers, 
etc. The sanatoriums in these and other regions combine the advan- 
tages of strict disciplinary supervision of out-door life, rest, exercise, food, 
bathing, clothing, medicinal and other treatment ; they are especially 
serviceable in early cases; and since they also exercise an educational 
influence not only upon the patients, but also among the people of their 
vicinity, their further establishment should be encouraged. 

If the patient has fever, that is, if the highest daily temperature is 
above 99.5° to 100° F., he should be at rest in bed, or at least in a reclining 
(steamer) chair. In the absence of fever, properly regulated, supervised, 
and graduated exercise should form a part of the general management. 
This may consist of walking, graduated ascents (as is used in German 
sanatoriums), or various sorts of light out-door work, the results of 
which, that is, the reaction of the patient to which (temperature, 
pulse-rate, weight, etc.), must be carefully noted. These exercises, as 
a rule, are most advantageously prescribed in the morning hours. 

Since the cure of tuberculosis depends upon the maintenance and improve- 
ment of nutrition, the greatest attention must be paid to the diet and the 
digestion. The food must be readily digestible, nutritious, varied, and 
appetizing, and it should be partaken of in stated amounts at stated 
intervals. An amount in excess of that which would be taken in health 
is necessary, but the excessive hyperalimentation in vogue several years 
ago seems undesirable. The diet should consist largely of milk, cream, 
butter, eggs, fish, bread, meats (especially beaf, mutton, chicken, and 
bacon), olive oil and other fats, etc. In addition to what might be con- 
sidered a goodly amount of a varied diet, the patient should take daily 
from one and one-half to two quarts of milk and from four to six eggs. 
Many patients do best by taking for breakfast some fruit,a cereal, bacon, 
t wo eggs, and milk (hot, if desired, and flavored with coffee, tea, or cocoa); 
:" full meal, for dinner, in the middle of the day, consisting, for instance, 
of soup, fish, meat, two or three vegetables, a salad, and fruit, a simple 
pudding or oilier dessert, or cheese; and for supper, in the evening, some 
cold meat, or fish, or two eggs, and toasted bread, boiled rice, or stewed 
fruit, and milk as at breakfast. The additional milk and eggs may be 
given between breakfast and dinner, between dinner and supper, and 



TREATMENT OF TUBERCULOSIS 129 

just before retiring for the night; with the milk it is advisable to take 
several crackers or a small amount of toasted bread to assist in com- 
minuting the curds. If the milk and eggs prove nauseating to the patient, 
they may be flavored, as already suggested, with coffee, tea, cocoa, or 
with chocolate, sodium chloride or bicarbonate, or a small amount of 
brandy, whiskey, port wine, sherry wine, etc.; and from time to time 
they may be discontinued for a day or two. Peptonization of the milk 
is sometimes serviceable for a time; or one may give kefir, koumiss, etc. 
Rarely it may be necessary to resort to Debove's method of forced feeding, 
which consists of preliminary washing of the stomach, followed by the 
introduction through the stomach tube of a quart of milk, one or two eggs, 
and three ounces of finely minced meat; this is done three times a day. 
A raw-meat dietary (zomotherapy), consisting of the use of one to two 
pounds or more of meat daily, either minced and raw, or made into a 
soup, has been readvocated lately. Anorexia and nausea are sometimes 
deterrents to proper feeding; but several days of life in the open air, or 
a change of scene, or an ocean voyage usually act as an efficient tonic to 
a jaded appetite. Sometimes, however, it may be necessary to admin- 
ister tonics; but care must be exercised that medicines employed for 
other purposes do not derange the stomach. Alcohol, as a rule, is not 
indicated: indeed, most patients do better without it altogether; but there 
can be no serious objection to a small amount of brandy or wine to flavor 
the milk and eggs from time to time. In advanced cases with fever, 
emaciation, rapid pulse, night sweats, poor digestion, etc., alcohol 
seems to do good; at least it aids digestion, especially the digestion and 
assimilation of fats, stimulates the heart ,and the nervous system, pro- 
motes a feeling of well being, relieves the night sweats, induces sleep, and 
if it does not lead to fibrosis, as has been claimed, it does not accelerate 
the progress of the lesions. 

Specific Remedies. — Tuberculin is a valuable adjuvant to other 
forms of treatment in selected cases. The preferable preparations are: 
Koch's new tuberculin, tuberculin residue (T. R.), consisting of the 
toxins and endotoxins of crushed tubercle bacilli unchanged by heat or 
chemicals; bacillen emulsion (B. E.), which consists of one part of finely 
pulverized virulent tubercle bacilli and one hundred parts each of dis- 
tilled water and glycerin; and Deny's bouillon filtre (B. F.), which con- 
sists of a filtrate from a bouillon culture and contains all the soluble toxic 
and other products of the tubercle bacillus. The cases suitable for 
tuberculin treatment are the early cases with circumscribed lesions, in 
which there is little if any fever or emaciation, and no excavation, and 
chronic cases with good nutrition and no serious complications; distinct 
contra-indications comprise rapidly advancing lesions, hectic fever, 
rapid heart action, and progressive emaciation. Trudeau advises: to 
begin with small doses, such as yolro o milligram (liquid measure) of the 
bouillon filtre (B. F.); to avoid provoking local or general reactions; to 
increase the dose gradually, at intervals of three or four days, or longer 
when large doses are given, until a maximum dose of 1 c.c. of the tuber- 



130 BACTERIAL INFECTIONS 

culin is reached; in case a reaction occurs, especially if this be associated 
with fever and constitutional disturbances, to reduce the next dose to 
about half of that which induced the reaction; and to continue the treat- 
ment for months, but not indefinitely for fear of exhausting the patient's 
power to respond, by the formation of antibodies, to the stimulus of the 
injection: it being better to discontinue the treatment for from three to 
six months and resume it again if anything in the patient's symptoms or 
condition seems to make this necessary. 

Medicinal Agents. — The medicinal treatment of tuberculosis is 
largely symptomatic; but certain remedies are given with the view to 
improve nutrition and increase the powers of resistance of the individual. 
Of these, the most valuable are arsenic, especially in the form of Fowler's 
solution, 5 minims (0.30 gram) three times daily; mercuric bichloride or 
succinimide, ^ to A" g ram (0.005 to 0.0018 gram) three times daily; 
strychnine, cod-liver oil, iron, the hypophosphites, etc. Inunctions of 
europhen (5 per cent, in olive oil) and other iodine preparations also 
have been commended. 

While the symptoms of tuberculosis are commonly improved by fresh 
air, nutritious food, regulated rest and exercise, they sometimes demand 
special attention. Cough, unless excessive, need not be restrained 
medicinally; often it can be repressed mentally; since, however, it serves 
to remove secretion, it is to some extent a necessary evil. In general, 
if requiring treatment, it should be met with the measures mentioned 
under bronchitis. Creosote is a very valuable remedy, and may be given 
in doses beginning with 3 minims (0.18 gram) and gradually increasing, 
three times daily, in milk, hot water, brandy, or a bitter tincture. Guaia- 
col carbonate is sometimes better borne. The distressing nocturnal 
cough may be controlled by the following: 

fy — Codeine 3 grains 20 

Dilute hydrocyanic acid 24 minims 1 50 

Glycerin 1 ounce 30 00 

Cherry laurel water, sufficient to make 3 ounces 100 00 — M. 

S - — Two teaspoonfuls (10 c.c.) at 6 and 9 p.m., and during the night if necessary. 

Comfort is sometimes promoted by diffusible stimulants, such as 
Hoffman's anodyne, spirit of chloroform, etc., or by hot whiskey on 
retiring; in other cases morphine may be required, but it should be given 
cautiously in the event of cavity formation, since the cavities must be 
emptied. Inhalations are often of marked benefit. Beverley Robinson 
extols the virtues of equal parts of creosote and alcohol, or, when there is 
much irritative cough, equal parts of creosote, alcohol, and spirit of 
chloroform (on an inhaler). Lees advocates the use of six to eight drops 
of the following on an inhaler, every hour during the day, and two or 
three times during the night, if the patient is awake: 

$— Carbolic acid 2 drams 8 

Creosote 2 drams 8 

tincture of iodine 1 dram 4 

Spirit of ether ! dram 40 

Spiril of chloroform 2 drams 8 Q-M. 



DIPHTHERIA 131 

The treatment of hemoptysis is discussed on page 540. Pleural 
pains may be relieved by counterirritation with tincture of iodine to 
which a small amount of croton oil may be added; by a blister; by rubbing 
with a mixture of equal parts of menthol, camphor, and chloral; or by 
strapping the side. The night sweats may be controlled by an abundance 
of fresh air at night, and the avoiding of too many bed-clothes; by sponging 
the body with alcohol and alum water; and by the use of camphoric 
acid, 20 to 40 grains (1.3 to 2.5 grams), four hours before the time of the 
expected sweat; atropine, y^- to yj-g- grain (0.0004 to 0.0006 gram) at bed- 
time; picrotoxin, -yj-g- grain (0.0006 gram), aromatic sulphuric acid, agara- 
cin, etc. In the event of fever, the patient should be at rest in bed. Rest 
in bed, fresh air, and nutritious food comprise the best treatment for the 
fever as such; but should the fever become high, attention should be 
paid to a sufficiency, but not an excess of bed-clothes; the body should 
be sponged repeatedly with cool water or with alcohol and alum water. 
Quinine, the salicylates, and the coal-tar products are distinctly contra- 
indicated; of course, they may reduce the temperature, but at the expense 
of the bodily resistance. Painful dysphagia may be relieved by spraying 
the throat with cocaine (2 per cent.) or by swabbing the throat with 
orthoform (5 per cent.) in olive oil. The treatment of so-called dys- 
pepsia and diarrhoea is similar to that mentioned elsewhere under these 
headings. 

Special Forms of Tuberculosis. — In miliary tuberculosis, treat- 
ment is of very little avail. Supportive 'measures are indicated, espe- 
cially strychnine, whiskey, camphor, etc., and in the event of restlessness, 
headache, and other cerebral symptoms, the bromides and opiates. In 
the event of meningitis lumbar puncture by relieving pressure may lead 
to amelioration of the symptoms; other measures mentioned under 
meningitis may be resorted to. The treatment of acute tuberculous 
pneumonia is that of pneumococcic infection of the lung, together with 
such of the aforementioned measures as may seem indicated when the 
tuberculous nature of the disease has been recognized. The treatment 
of many forms and localizations of tuberculosis is distinctly surgical : for 
instance, tuberculosis of the lymph nodes, of the serous membranes, of 
the skin, of the bones and joints, etc. Recourse has also been had to 
surgical intervention in certain cases of localized tuberculosis of the lung 
and with some encouraging results, details of all of which may be found 
in books of surgical practice. 

DIPHTHERIA. 

Diphtheria is an acute, specific, infectious, and highly contagious 
disease caused by Bacillus diphtherias (Klebs-Loffler), and characterized 
by fibrinous (croupous, or diphtheritic) inflammation of a mucous 
membrane, fever, and divers manifestations of toxemia. 

Etiology. — Diphtheria is peculiarly a disease of childhood, occurring 
most frequently between the second and the fifth year, and attacking 



132 - BACTERIAL INFECTIONS 

the sexes equally (under similar circumstances). It is relatively infre- 
quent after the tenth year, but adolescents and adults (nurses, physicians, 
attendants, etc.) are rather commonly affected and often succumb. The 
disease occurs in almost all parts of the world, but is especially prevalent 
in the temperate zone. It is endemic in most large cities, and frequently 
prevails epidemically, especially during the colder months of the year — 
the late fall, the winter, and the early spring; but the epidemics vary 
considerably in severity. In some sections the disease is relatively more 
common in the country districts than in the cities. General insanitary 
conditions are of etiological significance only in so far as they reduce 
the vitality of the individual and favor the harboring and multiplying 
of the bacilli. Overcrowding, such as obtains in schools, asylums, 
tenements, etc., is of significance in permitting the ready dissemina- 
tion of the bacilli among large numbers of susceptible persons. One 
attack confers an incomplete and temporary immunity. Recurrences 
are not infrequent. 

The exciting cause of the disease is Bacillus diphtheria, which may 
be isolated from the local fibrinous inflammations, the secretions and 
discharges from the throat and nose, sometimes from the blood and the 
internal organs, especially the lung (in the event of bronchitis and 
bronchopneumonia), but also the liver, spleen, kidney, etc. The disease 
is highly contagious and spreads with considerable rapidity. Infection 
may be transmitted by direct inoculation; by contact or proximity; 
by a third person (physicians, nurses, in whose hair the bacilli have been 
found, etc.); by fomites, especially room furnishings, room dust, bed- 
linen, personal linen, dishes, toys, etc., to which the bacilli often cling 
for a long time; by infected food and drink, especially milk (answerable 
for a number of epidemics), cheese, etc.; by domestic animals, etc. 
Infection is usually acquired by inhalation or swallowing, but it may also 
be acquired through a wound or abrasion. Individual susceptibility 
is of much etiological significance : many persons exposed to the infection 
do not acquire it, and others harbor the bacilli in their throats, and them- 
selves escaping infection, often disseminate it. In the throats of con- 
valescents, for instance, the bacilli may remain virulent for a long time 
(weeks and months) — so-called " chronic carriers," responsible for many 
outbreaks. Chronic nasopharyngeal catarrh, enlarged tonsils, carious 
teeth, etc., also favor infection. 

Pathology. — The characteristic lesion is the so-called false membrane, 
the relative frequency of the situation of which is well exemplified by the 
results of the investigations of Councilman, Mallory, and Pearce, who, 
among 127 of 220 fatal cases, found it situated as follows: In the larynx, 
75 ; trachea, 66 ; tonsils, 65 ; epiglottis, 60; pharynx, 51 ; nasal mucous mem- 
brane, 43; bronchi, 42; soft palate, including uvula, 13; oesophagus, 12; 
tongue, 9; stomach, 5; vagina, 2; duodenum, 1 ; vulva, 1; skin of the ear, 
1 ; conjunctiva, 1. Thus, in fatal cases the larynx is most frequently in- 
volved ; but this is not true of all, especially non-fatal cases, in the majority 
of which the tonsil is first and most frequently attacked. This' false 






DIPHTHERIA 133 

membrane -may be circumscribed in extent or widespread. Sometimes it 
is limited to a small region of the tonsil or soft palate; in other cases it 
covers the tonsils, soft palate, pharynx, larynx, and trachea; it may 
extend to the nose (which may become completely obstructed), to the 
conjunctiva (through the tear duct), and to the accessory sinuses (which, 
as pointed out by Councilman, Mallory, and Pearce, are very frequently 
involved, and the unhealed lesions of which are often answerable for 
the persistence of diphtheria bacilli in the nose and throat). It may 
travel through the Eustachian tube to the middle ear, over the tongue, 
and involve the oral mucous membrane, through the bronchi to their 
finest ramifications, through the oesophagus to the stomach, intestine, 
etc.; and by transference it may implicate other mucous membranes, 
such as the vulva, vagina, etc. In character, the membrane varies con- 
siderably: it may appear as a thin, whitish, more commonly grayish or 
fawn-colored, pellicle, easily removable without loss of substance or 
bleeding; or it may present all gradations of severity from this to a dense, 
tough, grayish, brownish, or blackish membrane, firmly attached in the 
early stages and separable only with difficulty and leaving a bleeding- 
surface, but later softer and more shaggy; or the lesions may be markedly 
necrotic or really gangrenous. The membrane is more easily removed 
from the trachea and larynx than elsewhere, being sometimes expelled 
by coughing, and it rarely occasions in these regions a loss of sub- 
stance extending beyond the superficial epithelium; the subepithelial 
layer, however, is always markedly injected. 

Councilman, Mallory, and Pearce, who have studied the lesions atten- 
tively, describe them as follows: The earliest lesions are due to the 
toxin, produced by the diphtheria bacillus, possibly growing in the fluids 
of the mouth and throat. The toxin gives rise to degeneration and necro- 
sis of the epithelium, often preceded by active proliferation of the nuclei 
of the cells by direct division. In this necrotic tissue, but more especially 
in the exudate speedily formed, the bacilli become implanted and there 
continue their deleterious action; but the bacilli themselves are not 
found growing in living tissue. "The cells may either break up into a 
detritus, with fragmentation of the nuclei, or they may become changed 
into refractive hyaline masses. An inflammatory exudation rich in 
fibrin factors comes from the tissue below, and fibrin is formed when this 
comes in contact with the necrotic epithelium. The fibrin in part is 
formed into a reticulum around exudation cells and degenerated epi- 
thelium, in part, it combines with the hyaline degenerated cells to form 
a hyaline membrane. It is probable that a hyaline membrane may 
be formed without the exudation; in this case the network of the mem- 
brane represents the edges of the cells, and the spaces the former 
nuclei. The hyaline membrane is most often formed on those surfaces 
which are covered with epithelium having several layers of cells. It 
may be formed by a hyaline degeneration of exudation cells; in this 
case the spaces in the meshwork are smaller. It is probable that the 
fibrinous membrane is formed both on the surfaces and in the tissue. 



134 BACTERIAL INFECTIONS 

The fibrin is first formed around cells that afterward disappear. In 
the trachea the fibrinous membrane often has a definite structure. 
The membrane may disintegrate and be broken up into a mass of 
detritus (the process commences on the surface), or it may be cast 
off as a whole by being elevated by an exudation beneath. Very 
thick masses of membrane may be formed by the constant addition of 
fibrinous exudation. The membrane is never formed primarily on an 
intact epithelial surface, but it may extend over it. Nothing is to 
be gained by making an anatomical distinction between a croupous 
and a diphtheritic membrane. . . . The membrane formation 
is accompanied by changes in the tissue beneath, which represent a 
combination of degeneration and exudation. The connective tissue 
and bloodvessels undergo a hyaline fibrinoid degeneration very similar 
to the degeneration of the epithelium. Necrosis may extend deeply 
into the tissue, but there is little tendency to deep ulceration or abscess 
formation. The degeneration in the mucous glands of the tissue is 
so pronounced as to be almost specific. Marked degeneration of the 
epithelium of the glands may be found without any change in the 
surrounding tissue." 

The organs in general show lesions common to most of the toxemias. 
In the kidneys the lesions vary from cloudy swelling to severe nephritis. 
In the liver the degenerative changes are not so marked, nor are they 
specific. The spleen is sometimes enlarged. The lymph nodes, 
especially those nearest the primary lesions, show changes — of two 
kinds: (1) Congestion, hemorrhage, and diffuse and circumscribed 
necrosis — found in many conditions; and (2) foci of proliferation, 
phagocytosis, and degeneration, resembling tubercles — distinctive of 
diphtheria, but found also in other conditions. Degeneration of the 
myocardium is common; it is usually fatty, sometimes hyaline. Acute 
interstitial myocarditis, endocarditis, and pericarditis also occur. 
Bronchopneumonia (acinous pneumonia, Councilman, Mallory, and 
Pearce) is found in more than half of the fatal cases. Peripheral neu- 
ritis (cranial and spinal) is common and answerable for many of the 
serious sequels. Poliomyelitis and hemorrhage into the cord and 
membranes are also encountered. 

As already stated, general infection with the diphtheria bacillus 
(Contrary to former opinions) is not uncommon, especially in the fatal 
cases; but .in these cases there is usually also associated infection with 
the streptococcus (the most important and most common), the staphy- 
lococcus, the pneumococcus, etc. These organisms are also frequently 
found associated with the diphtheria bacillus in the local lesions in the 
throat and in the complications, especially the bronchopneumonias 
and the suppurations. These cases of mixed infection are often unusu- 
ally severe clinically, and not infrequently terminate fatally — the one 
bacterium apparently assisting the other in producing the severe mani- 
festations of the infection. 



DIPHTHERIA 135 

Variations in Virulence of the Diphtheria Bacillus — Avirulent Diphtheria 
Bacilli. — I have already said that the diphtheria bacilli may be found 
in the throats of healthy persons, and, sometimes for a long time, in 
the throats of convalescents. It is sometimes found also in throats 
in which the lesions are only a mild catarrhal tonsillitis or faucitis or 
a lacunar tonsillitis. The diphtheria bacilli, thus, vary considerably 
in virulence: some are slightly, if at all, virulent, that is, they produce 
little if any toxin (attenuated bacilli); others are more virulent, but 
the resistance of the individual is good and he escapes serious infec- 
tion, though he may transmit serious and even fatal infection to others 
or give rise to a more or less widespread epidemic. In other cases 
bacilli are found that resemble the diphtheria bacillus more or less 
closely morphologically, but differ from it biologically — bacilli often 
ill-advisedly spoken of as the pseudodiphtheria bacillus, Bacillus 
xerosis (found in the healthy and diseased conjunctiva), and bacilli 
found also in many other places and conditions. 

Diphtheroid Infections. — Whereas the diphtheria bacillus is the most 
common cause of pseudomembranous inflammation, it is absent in 
some cases, the causative agent being usually the streptococcus, occa- 
sionally the pneumococcus, the staphylococcus, and sometimes appar- 
ently other organisms ill understood and cultivated with difficulty, 
if at all, in artificial media (such as Vincent's bacillus, etc.). The 
preferable designation for these conditions is streptococcic, pneumo- 
coccic, or staphylococcic angina, tonsillitis, faucitis, etc. In view, how- 
ever, of the occurrence of necrosis and fibrinous exudation they are 
not infrequently confounded with true diphtheria, and are sometimes 
spoken of as pseudodiphtheria, secondary diphtheria, diphtheroid, 
etc. Diphtheroid infection is the least objectionable of these, but it 
should be replaced by the other terms suggested. Thus, there is not 
infrequently a discrepancy between the clinical and the bacteriological 
diagnosis, some cases clinically diphtheria are provoked by other micro- 
organisms, and certain other cases clinically very mild, with little, 
if any, membrane, are examples of true diphtheria. The many note- 
worthy additions to our knowledge during recent years, however, have 
led to a gradual revision of our conception of many morbid processes, 
and to the establishment of certainty and exact knowledge where formerly 
uncertainty and doubt were common; witness, for instance, the practical 
abandonment of the idea of "croup" as a distinct and separate entity. 

These diphtheroid (streptococcic, staphylococcic, pneumococcic, etc.) 
infections or inflammations may occur: (1) As independent disorders, 
varying much in frequency, but sometimes, according to Park and 
Beebe, constituting as much as 40 per cent, of the then existing sore 
throats. They are only slightly (if at all) contagious; the symptoms, 
as a rule, are much milder than those of true diphtheria, and the 
mortality is much less — not more than 2.5 per cent. (Park and Beebe). 
(2) As secondary infections in several of the infectious diseases, especially 
scarlatina, measles, pertussis, typhoid fever, etc. The symptoms are 



136 BACTERIAL INFECTIONS 

often severe, and through the supervention of general pyococcic infection 
not infrequently lead to death. Of course, true diphtheria also may 
complicate any of these or other infectious diseases. 

Symptoms. — The period of incubation in true diphtheria varies from 
two to seven days, but in severe infections it may be scarcely more than 
twenty-four hours. As a rule, prodromes are slight or absent — consist- 
ing, when present, of general indisposition and disinclination to play, 
and possibly headache. The onset of the disease is usually gradual, 
the child complaining of increasing headache, apathy, general neuro- 
muscular pains and aching, slight chilliness, and fever which soon 
reaches 102° to 103° F. Occasionally the onset is abrupt — with con- 
vulsions or vomiting and fever (103° to 104° R). The subsequent 
local and general manifestations of the infection vary considerably, 
depending upon the virulence of the microorganisms, the localization 
of the process, and the local and general resistance of the patient. 

In 'pharyngeal or faucial diphtheria there is usually more or less 
complaint of sore throat or of pain on swallowing; but in many cases 
the absence of such complaint is noteworthy. On inspecting the 
throat (a procedure that should never be neglected in sick children) 
the tonsils are found swollen, reddened, often peculiarly cyanotic, 
and a small patch of false membrane — whitish, grayish, or fawn-colored 
— may be visible. This forms, as a rule, first on one or the other tonsil, 
but soon involves adjacent structures. In some cases the pseudo- 
membrane remains for some time undetected, having formed in regions 
not apparent to inspection, such as the posterior surface of the uvula, 
the recesses of the faucial pillars, etc. In these cases the disease, for 
the time being, is scarcely to be distinguished from an ordinary ton- 
sillitis. 

In mild cases the membrane remains confined to the tonsils, the 
uvula, and the soft palate. Frequently it may be removed with little 
loss of substance (or bleeding), but usually attempts to remove it result 
in exposing a raw-looking, bleeding surface — which soon becomes 
recovered. The fever is moderate (102° R), the pulse somewhat 
accelerated (about 100 in children three or four years of age); the sub- 
maxillary glands are slightly, if at all, swollen, and the evidences of general 
intoxication are slight. There is usually a moderate leukocytosis and a 
trace of albumin in the urine. At the end of four to six days the fever 
begins to subside, and the membrane to shrivel, to curl up at the edge, 
and gradually to separate. By the eighth or ninth day it is usually 
gone, but the surface may remain red and inflamed for some time. 

In cases of moderate severity, the false membrane is more widespread 
and deeper, inflammatory oedema and congestion are more marked, 
the submaxillary glands are considerably swollen, the appetite is lost, 
the fever is high (103° to 104° P.), the pulse is rapid (110 to 120), the 
urine is lessened in amount and contains albumin and casts, prostration 
is quite marked, and the child is more or less restless and delirious. 



DIPHTHERIA 137 

These cases not infrequently eventuate in death, but recovery may 
ensue at the end of ten days or two weeks. 

In severe cases (malignant diphtheria) the child is usually quite ill from 
the beginning (but cases beginning mildly may become severe) ; vomiting, 
convulsions, and high fever may usher in the attack. The pharyngeal 
tissues become intensely cedematous, reddened, and swollen, the tonsils 
often meeting in the median line ; the faucial tissues become covered with, 
apparently converted into, a grayish, brownish, or greenish-black, ragged, 
malodorous membrane or slough-like mass; a fetid, watery, or sanious 
discharge issues from the nostrils and the mouth; the submaxillary and 
other regional lymph nodes become much swollen and assist in quite 
fixing the jaw; the face, later the neck and chest, become swollen and 
cedematous, and in some cases a pallid lividity of the general integument 
supervenes. The fever may be quite high or remarkably low, even per- 
sistently subnormal (bad prognostically) ; the pulse is rapid, irregular, 
and weak, the respirations embarrassed and noisy (open mouth and 
obstructed throat); the urine is much diminished in amount and con- 
tains much albumin and many casts; and marked prostration, stupor, 
and delirium develop. An erythematous or purpuric rash is not 
uncommon; hemorrhages may issue from the nose or mouth, and con- 
tribute to a speedy fatal issue; or extensive sloughing and gangrene 
of the neck (Ludwig's angina) may ensue. Death usually results in 
from three to eight days from toxemia, cardiac and vasomotor paralysis, 
or certain complications. 

Nasal diphtheria may occur as a primary disorder and later spread 
to the throat, or it may develop secondarily to faucial diphtheria. It 
may be mild, severe, or malignant in type. There may be little if any, 
membrane — only a profuse seros anguine ous discharge, which quite 
naturally excoriates the upper lip (formerly believed to be of much diag- 
nostic significance); or the membrane may be so marked as completely 
to occlude the nares. Glandular enlargement is usually marked (owing 
to the rich lymphatic supply of the nose), and the constitutional dis- 
turbances (prostration, albuminuria, delirium, etc.) are usually severe. 
In most cases of pharyngeal diphtheria the diphtheria bacillus may be 
cultivated from the nasal secretions, even in the absence of noteworthy 
lesions in the nose. 

Fibrinous rhinitis is a curious disorder, subacute or chronic in course, 
characterized by recurring thick fibrinous exudation, benign in nature, 
and attended by slight constitutional disturbance — but due in 80 per 
cent, of the cases (RaveneFs collection of statistics) to the diphtheria 
bacillus. 

Laryngeal diphtheria (formerly so-called membranous croup) develops 
usually secondarily to pharyngeal diphtheria, but it may occur as a 
primary disorder, and, as previously mentioned, laryngeal lesions are 
the most common in the fatal cases. In the majority of cases, the 
symptoms in the beginning are not unlike those of pharyngeal diphtheria 
— but the voice soon becomes hoarse, a rough, brassy, or "croupy" 



138 BACTERIAL INFECTIONS 

cough develops, and the respirations become embarrassed. At the 
end of twenty-four or forty-eight hours, commonly at night at first, 
evidences of laryngeal or bronchial obstruction (stenosis) develop sud- 
denly. At first these are often paroxysmal (spasm of the glottis), 
but later they become continuous (increasing mechanical obstruction). 
The inspiratory and expiratory efforts are attended by unusual efforts ; 
they become loud and stridulous, and are associated with retraction 
(on inspiration) of the intercostal spaces and the epigastrium; the 
child becomes extremely restless and makes extraordinary efforts to get 
air, and becomes cyanotic and markedly prostrated. In the beginning 
these attacks sometimes subside spontaneously; in other cases they are 
relieved by coughing and the expelling of a portion of false membrane 
(sometimes casts of the larynx or a bronchus); in most cases, how- 
ever, unless relieved, the dyspnoea and cyanosis become aggravated and 
continuous, restlessness, which at first becomes more marked, is gradually 
replaced by stupor and coma, prostration increases, and the child dies 
of asphyxiation. In some cases, in which the false membrane extends 
to the bronchi, death from suffocation may be comparatively slow. 
If the pharynx is not much involved, the evidences of toxemia at first 
are slight (on account of the poor lymphatic supply of the larynx), the 
fever is slight or moderate, and the general condition of the child is good 
— until the onset of the laryngeal obstruction. In laryngeal diphtheria, 
therefore, there is usually a marked disproportion between the severity 
of the local and the general symptoms. 

Wound diphtheria occasionally occurs — when the diphtheria bacilli 
become implanted in a wound; but not all membranous inflammations 
of wounds are diphtheritic. Diphtheria occasionally occurs also on 
other mucous membranes, such as the conjunctiva, the vulva, vagina, 
anus, etc., and as a primary or a secondary infection. 

Complications and Sequels. — The most important complications 
(due usually to pyogenic organisms associated or not with the diph- 
theria bacillus) are: Severe and even fatal hemorrhage from the nose 
and throat; bronchitis, bronchopneumonia (acinar pneumonia), and 
pulmonary atelectasis; suppuration of the lymph nodes; otitis 
media and disorder of the accessory sinuses of the nose; Ludwig's 
angina; cutaneous rashes (erythema, urticaria, purpura, gangrene); 
endocarditis; arthritis (simple and suppurative); suppression of urine 
and nephritis; general pyemia with metastatic abscess formation 
(secondary pyococcic infection). Diphtheria may also complicate 
certain of the infectious diseases, especially scarlatina, pertussis, measles, 
typhoid fever, tuberculosis, etc. 

The most important sequels are the paralyses — which occur in about 
20 per cent, of the non-fatal cases, are due to a toxic peripheral neuritis, 
and occur usually during the second or the third week of convalescence, 
though they may come on as early as the seventh or eighth day of the 
disease. The most common are: Paralysis of the palate (return of 
fluids through the nose, difficulty in swallowing, a nasal quality to the 



DIPHTHERIA 139 

voice, relaxation and impaired sensation of the palate) ; of the internal 
muscles of the eye (paralysis of accommodation) ; of the external muscles 
of the eye (ptosis, strabismus); of the facial muscles; of the laryngeal 
muscles (unilateral or bilateral); of the extremities or trunk (paresis, 
paresthesias, incoordination, loss of reflexes); and of the diaphragm. 
These usually subside in from two weeks to two months. The most 
serious paralysis involves the heart and the vasomotor system. This 
may result not only from toxic degeneration of the nerves supplying 
the heart, but also of the vasomotor nerves, and from toxic myocarditis, 
heart clot, etc. It may come on as late as two months after apparent 
convalescence, and may follow apparently mild attacks of diphtheria, 
though it is more common after severe attacks. Many of the deaths 
occurring during the course of diphtheria are due to this cardiac and 
vasomotor paralysis. The pulse is often slow rather than rapid; it 
becomes weak, the temperature sinks, the skin becomes pale, and the 
child soon dies. During convalescence death from this cause may 
occur suddenly, and entirely unannounced; it not infrequently follows 
immediately some unusual exertion. It is sometimes preceded by 
a warning arrhythmia, vertigo, vomiting, and signs of cardiac dilatation. 
Anemia often persists for a long time. Nephritis, laryngeal stenosis, 
chorea, etc., have been observed as sequels. 

Diagnosis. — In many cases the diagnosis depends upon the demon- 
stration of the diphtheria bacillus — which is conclusive. Provision 
for the ready and prompt determination of the bacteriological factor 
in cases of sore throat is now commonly made by the establishment of 
municipal and State laboratories; in the absence of these, private labora- 
tories are usually available. But what is still better — the physician 
should train himself to make the necessary simple examination. A 
properly prepared cover-slip preparation will, in the majority of cases, 
within a few minutes convert doubt into certainty. Cultures also should 
be undertaken. Such examinations should be made in all cases of sore 
throat, since, as already mentioned, many cases mild clinically are truly 
diphtheritic and act as sources of infection. In the event of doubt 
all throat disorders in children should be regarded as diphtheritic, 
and the proper prophylactic and curative measures should be instituted 
immediately. Pending the detection of the diphtheria bacillus, the 
presence of an epidemic (or exposure to infection), the characteristic 
false membrane, a sanious discharge from the nose or the mouth, swell- 
ing of the submaxillary lymph nodes, and albuminuria are of much 
diagnostic value. 

Streptococcic, staphylococcic, pneumococcic, and other pseudo- 
membranous anginas (such as Vincent's angina, etc.) often can be 
excluded only by bacteriological examination; but in these the onset is 
usually more sudden than in diphtheria, the fever is higher and of shorter 
duration, glandular enlargement is less, albuminuria is often absent, 
there is less tendency for the lesions to spread to the nose and the larynx, 
and there is no history of exposure to diphtheritic contagion. In 



140 BACTERIAL INFECTIONS 

scarlatina the throat lesions sometimes become "diphtheroid," and 
may not be distinguishable from those of true diphtheria except by 
bacteriological examination. Diagnostic difficulties are sometimes 
enhanced by an erythematous rash that occasionally occurs in diph- 
theria. However, this is uncommon, and is darker and of shorter dura- 
tion than the true scarlatinous rash, and it is usually confined to the 
trunk. The two diseases not infrequently co-exist. In follicular ton- 
sillitis the exudate is yellowish (rather than grayish or fawn-colored), 
patchy (corresponding to the follicles), is separated by intervening 
areas of congested red tonsillar tissue, does not tend to spread beyond 
the tonsils, may be removed without leaving a bleeding surface, and 
does not tend to reform (as in diphtheria). Spasmodic laryngitis, 
"false croup," "spasmodic croup" can scarcely be confounded with 
diphtheritic laryngitis ("true croup"). 

Prognosis. — The prognosis varies with the severity of the infection, 
the reaction of the individual, the presence or absence of complications, 
and especially with the treatment adopted. In some epidemics the 
death rate has been as high as 50 per cent. Since the introduction of 
antitoxin it has been reduced at least one-half; and in some large series 
of cases the prompt use of antitoxin has reduced the mortality to between 
10 and 15 per cent. The prognosis is poorer in very young children, 
in the event of laryngeal and nasal involvement, marked toxemia, heart 
weakness, etc. The most marked discrepancies sometimes occur 
between the severity of the local lesions and the degree of systemic 
toxemia: minor local lesions are sometimes attended by very serious 
general manifestations; in some cases the patient is overwhelmed with the 
toxemia and dies within a day or two — before the local lesions have become 
noteworthy; while in still other cases well-marked and even extensive 
local lesions run their course without evidence of serious intoxication. 

Treatment. — Isolation and prophylactic measures of the strictest 
sort should be carried out (page 29). Special attention should be 
directed to mild cases, ambulatory cases, convalescents (in whose throats 
virulent bacilli may remain for from six weeks to six months or more 
after the attack), and to attendants upon the sick. Catarrhal disorders of 
the nasopharynx, especially in children, should be corrected. Children 
exposed to infection should be required to use mild antiseptic nasal, 
oral, and pharyngeal washes (boric acid, potassium permanganate 
0.5 to 1 per cent., mercuric bichloride 1 to 10,000), and should be given 
a prophylactic dose of antitoxin, 200 to 500 or 1000 units, depending 
upon its age. 

The general hygienic and dietetic management of the developed 
disease is similar to that appropriate in the other infectious diseases 
in children. It is important, however, that the diet throughout should 
be fluid, concentrated, and readily digested. In the event of intubation 
or tracheotomy being necessary, rectal alimentation may be required. 

The diagnosis of diphtheria brings with it the imperative indication 
for the use of the specific remedy— antitoxin. Even in case of doubt 



DIPHTHERIA 141 

as to the true nature of a throat disorder it is wise to administer diph- 
theria antitoxin — since in the event of the disease proving to be diph- 
theria the proper remedy has been administered at the most opportune 
moment, and in the event of its proving to be non-diphtheritic in nature, 
no harm has been done (indeed, possibly some good). The proper 
dose of antitoxin is that sufficient to insure the desired result; it is 
much better to give more than is really necessary than too little. In 
mild cases in children over two years of age, 3000 to 4000 units, and 
in severe (including laryngeal) cases 4000 to 8000 units should con- 
stitute the initial dose. This should be repeated in from six to eight 
hours if the swelling and congestion are not lessened, and the membrane 
seems to maintain its tenacious hold, and in from four to six hours, 
if the local lesions seem to be progressive and the membrane to be 
spreading. In some cases a third dose may be required at the end 
of four to eight hours, or after the lapse of twenty-four or thirty-six 
hours; and in a few cases, even a larger number of doses. Dr. 
McCollom, of Boston, has obtained the most gratifying results, in 
apparently hopeless cases, by using as much as 70,000 units. Large 
doses given early usually obviate the necessity of using antitoxin at the 
end of a week or thereabout after the first dose, and thus remove all 
possibility of producing anaphylaxia. The use of globulin preparations 
(from which some of the non-antitoxic serum substances have been 
removed) tends to lessen the likelihood of disagreeable rashes developing. 
The antitoxin should be injected into the trunk or the thigh, and 
as early as possible (even pending the bacteriological report) ; but it is 
important to administer it no matter when nor how late the child comes 
under observation. The following statistics collected by Cohn illustrate 
the results of antitoxin treatment as influenced by the day on which it 
is commenced: 

Per cent. 

Patients. mortality. 

First day 78 13 

Second day 361 11.1 

Third day 284 10.5 

Fourth day 101 24.7 

Later and unknown 186 22.7 

Striking results often follow the use of the antitoxin. When admin- 
istered early, at the end of ten or twelve hours, the fever often abates, 
the local inflammatory oedema and congestion lessen, the pseudo- 
membrane begins to curl up at the edge and soon loosens, and the evi- 
dences of toxemia diminish. In some cases, aside from anemia and 
weakness, the patient is quite convalescent in two or three days. The 
local lesions, however, are of more significance as suggesting the renewed 
use of antitoxin than the general manifestations. When the antitoxin 
is administered late, the results are not so striking, but the severity of 
the local lesions and the general infection are undoubtedly mitigated; 
many patients who otherwise would require it are spared intubation 
and tracheotomy; many in whom otherwise tracheotomy would be 



142 BACTERIAL INFECTIONS 

required recover with intubation; the intubation tube may be removed 
much earlier than in pre-antitoxin days; and the mortality of intuba- 
tion and tracheotomy cases is reduced one-half. The antitoxin, being 
a specific remedy, does not influence the lesions due to associated organ- 
isms (streptococci, staphylococci, pneumococci, etc.), nor does it pre- 
vent complications and sequels, except in so far as it influences and 
mitigates the severity of the primary diphtheritic infection. 

Local treatment is advisable in most all cases, but it must be employed 
with discretion. The best treatment for the local lesions is the antitoxin 
internally; with no other remedy at our command are we so well able to 
destroy the diphtheria bacilli in the mouth, nose, and throat. Cleanli- 
ness, therefore, is the main object of local treatment. The best local 
treatment consists of irrigation through the nose or mouth, with a foun- 
tain syringe or a hand syringe, using physiological saline solution (than 
which nothing is better), or mild antiseptic solutions, such as boric acid; 
potassium permanganate, 1 per cent.; hydrogen dioxide, 10 to 20 per 
cent. ; carbolic acid, 0.3 to 0.5 per cent. ; mercuric bichloride, 1 to 10,000; 
formalin, 0.5 to 1 per cent., etc. These may be used every hour or two, 
depending upon the severity of the local lesions and the resistance of 
the child, remembering that the possible good that may be thus achieved 
may be more than counterbalanced by enfeebling results of the child's 
struggling. Sprays are likely to frighten the child, and are thus some- 
times objectionable. Many physicians are partial to applications 
applied directly to the lesions on a swab; these often render good ser- 
vice, but should never be entrusted to other than trained hands — 
the physician or a trained nurse. The best preparation is Loffler's 
solution: Menthol, 10; toluol, 36; solution of iron chloride, 4; and 
absolute alcohol, 60. The more old-fashioned preparation, consisting 
of tincture of iron chloride, 3; carbolic acid, 0.5; glycerin, 15; and water, 
15, is also excellent. Digestants such as papain and trypsin, etc., 
have been recommended, but I have not much faith in their efficacy. 
Gargles are of little use, since usually they do not reach the place 
where their action is desired. 

In the event of laryngeal diphtheria, much good results from the 
inhalation (by means of a steam tent or croup tent) of steam, medicated 
with salt, lime, or compound tincture of benzoin, or the inhalation 
of the fumes of subliming calomel. External applications to the throat, 
hot and cold, are sometimes grateful, but they as frequently annoy 
and embarrass the patient as they help him. If symptoms of laryngeal 
obstruction develop, and the child is not too weak, the effects of vomiting 
at dislodging the false membrane may be tried: syrup of ipecac, i to 
1 ounce (15 to 30 c.c); tartar emetic, J grain (0.03 gram), hot mustard 
water, etc. If no relief follows, intubation should not be delayed, 
and it should always be undertaken if dyspnoea, cyanosis, and restless- 
ness are increasing, and if retraction of the interspaces and of the epigas- 
trium shows the difficulty the child experiences in breathing. If intuba- 
tion does not afford relief, tracheotomy must be performed. 



INFLUENZA 143 

Alcohol seems to be a very serviceable remedy, especially when the 
infection is severe, the prostration marked, and the first sound of the 
heart has become weak. It may be given in doses varying from one 
to six ounces in the twenty-four hours. Strychnine also is valuable in 
some cases. The common heart tonics are not of much value, though 
apparently indicated on superficial observation; but in the event of 
collapse of the circulation they may be tried, especially the more diffu- 
sible stimulants. Previous to antitoxin days, tincture of iron chloride, 
calomel and other preparations of mercury, quinine, etc., enjoyed con- 
siderable reputation; they are sometimes valuable adjuncts, and are 
especially serviceable during convalescence (particularly the iron). 

The complications are to be treated on general principles. Prolonged 
rest in bed (three to six weeks) during convalescence is essential. 



INFLUENZA. 

{La Grippe; Grip; Epidemic Catarrhal Fever.) 

Influenza is an acute specific, infectious, and moderately contagious 
disease caused by Bacillus influenzae (Pfeiffer), and characterized by 
fever, catarrh of the respiratory and the gastro-intestinal mucous mem- 
brane, severe neuromuscular pains, and marked prostration. 

Etiology. — Although influenza is prone to attack adults, no age is 
exempt, and the sexes are affected about equally. While the most 
robust persons are frequently attacked, the disease finds its readiest 
victims among those debilitated by any cause, as well as among the 
aged, in whom it is frequently fatal. It usually prevails epidemically, 
especially during the late fall and the winter, and has been practically 
pandemic since 1889-90. The local epidemic visitation of the disease 
continues about six or eight weeks, during which time an extremely 
large proportion of the population may be affected. One attack does 
not confer immunity, since relapses are common. Some persons seem 
to be more or less immune naturally. 

The exciting cause of the disease is Bacillus influenza?, which may 
be found in the mucous discharges, and in the lungs and other organs 
in the event of complications. The disease is moderately contagious, 
infection being transmitted by direct contact, possibly by a third person, 
and by fomites; but the unusually large number of persons affected 
almost simultaneously is attributable to widespread aerial dissemination 
of the bacillus. In some epidemics the infection appears to have been 
spread by the ordinary channels of commercial intercourse. Infection is 
acquired by inhalation. 

Pathology. — Influenza is devoid of characteristic lesions, the lesions 
found consisting of catarrhal inflammation of the respiratory and the 
gastro-intestinal tract, and rarely of enlargement of the lymph follicles 
of the intestine and of the spleen. The complicating lesions exhibit 
nothing specific. 



144 BACTERIAL. INFECTIONS 

Symptoms. — The period of incubation is usually two to four days. 
The onset is sudden, with severe chill or chilliness, high fever (often 
104° to 105° F.), violent headache, especially about the eyes and the 
root of the nose, severe neuromuscular pains and tenderness, especially 
in the back and legs, catarrh of the respiratory mucous membrane, 
marked prostration, and depression of spirits. Depending upon the 
predominance of certain symptoms different types of the disease are 
described, but all gradations between the different types occur: (1) 
The respiratory type. In this, symptoms referable to catarrh of the 
respiratory tract are marked — coryza, conjunctivitis with excessive 
lacrymation, sore throat, hoarseness, harsh, dry cough. Sometimes the 
catarrh is more marked in, or confined to, the upper part of the respira- 
tory tract, sometimes to the lower. Occasionally hemoptysis is observed. 
As a rule, after a couple of days there is a little mucous expectoration, 
and the usual evidences of bronchitis. As convalescence sets in the 
sputum becomes mucopurulent in character, but a harsh dry cough 
often persists for a long time. (2) Gastro-intestinal type. In addition 
to the general manifestations, nausea and vomiting sometimes occur 
as initial symptoms; later, abdominal pain and diarrhoea are common, 
and sometimes lead to collapse. Jaundice has been observed, and the 
spleen may be enlarged. (3) Nervous type. In this the catarrhal symp- 
toms are relatively slight, but the neuromuscular pains, cutaneous 
hyperesthesia, sweating, and prostration are marked. Delirium and 
stupor sometimes supervene, and with continuation of the fever a typhoid 
state (typhoid type) develops. (4) A cardiac type, with feeble, rapid, 
and irregular pulse, sometimes progressing to serious cardiac embarrass- 
ment has been described. (5) A muscular or so-called rheumatoid type, 
with severe pains and tenderness in the back, extremities, and joints 
may occur. (6) A hyperpyretic type, and (7) an apyretic type also have 
been described. 

In most cases the initial high fever remits at the end of twenty-four 
hours, and subsequently pursues an extremely irregular course, varying 
much in different cases. As a rule, it falls by lysis and reaches the nor- 
mal in from three or four to eight days, but recurrence of the fever on 
slight provocation is quite common. With the decline of the fever, 
the severe neuromuscular pains, the headache, and the catarrhal symp- 
toms abate and the patient gradually convalesces, though marked 
prostration and occasional sweatings may continue for a long time, 
and relapses are quite common. A second attack may occur during 
the same epidemic. 

Complications. — Secondary infections are common. Although there 
is a true influenzal pneumonia, the frequent lobar pneumonia and 
bronchopneumonia are often due to mixed infection with the pneu- 
mocpccus and the streptococcus. Abscess and gangrene of the lung and 
pleuritis have been observed. Myocardial weakness and irregularity 
of the heart action is common, and may last for a long time. Brady- 
cardia also occurs. Endocarditis, pericarditis, and thrombophlebitis 



BACILLARY DYSENTERY 145 

are less common. Divers nervous complications, such as neuritis, 
meningitis, encephalitis, etc., as well as nephritis, otitis media, kera- 
titis, herpes labialis and other cutaneous manifestations, etc., have 
been reported. 

Treatment. — Rest in bed is the most important feature of the treat- 
ment, and should be insisted upon even in the mildest cases in the 
event of fever, since convalescence is much hastened by a few days' 
rest in bed, and the likelihood of complications and of sequels is much 
lessened. The patient should be isolated, if possible, and the mucous 
discharges should be disinfected. The diet should be light and easily 
assimilable. Aside from these measures the treatment is largely symp- 
tomatic, but should be always supportive. A warm bath or a hot 
mustard foot-bath, with an initial dose of Dover's powder (10 grains, 
0.6 gram) and a hot drink at night, often serve to relieve the distress. 
Additional relief may be afforded by any of the following every two or 
three hours for the first day or two: aspirin, 5 to 10 grains (0.3 to 
0.6 gram); quinine, 2 grains (0.13 gram), and salicin, 5 grains (0.6 
gram); salol, 5 grains (0.3 gram), and acetphenetidin, 2 grains (0.13 
gram), to which one may add small doses of Dover's powder, \ to J 
grain (0.015 to 0.03 gram), or camphor monobromate, 1 grain (0.06 
gram). Intense headache may be relieved by an ice-bag, caffeine, or 
the bromides. Rarely, especially in the event of very severe headache 
and of severe neuromuscular pains, it seems almost necessary to resort 
to the coal-tar products, but aside from the small doses of acetphenetidin 
already mentioned, their use must be attended by caution, since although 
they may relieve the subjective complaints, they only add to the already 
existing prostration. In many cases, stimulants are called for, of which 
the most valuable are whiskey, brandy, and especially strychnine, and 
the aromatic spirit of ammonium. The treatment of the catarrhal 
symptoms is similar to that suggested in acute coryza and bronchitis. 
The emunctories always require attention: mild diaphoretic remedies 
are valuable; the bowels should be opened freely; and the urine should 
be rendered copious by the generous use of water and mild alkaline 
diuretics. Especial care must be exercised in the cases of elderly sub- 
jects to prevent the development of complications, especially of broncho- 
pneumonia, the cause of many fatalities in the aged. During convalescence 
strychnine is often required for a long time, and the persistent irritating 
cough without expectoration may require codeine or heroin. 



BACILLARY DYSENTERY. 

Bacillary dysentery is a specific infectious disease, caused by Bacillus 
dysenterise (Shiga), and characterized by abdominal pain, frequent 
intestinal discharges containing mucus and blood, and a specific serum 
reaction. 
10 



146 BACTERIAL INFECTIONS 

Etiology. — It is now generally believed that the common, especially 
acute, dysentery of the tropics and temperate zones is due to Bacillus 
dysenterise, an organism discovered by Shiga and later studied by Flexner 
and his pupils. Several strains of the bacillus are now recognized, 
that most common in this country being known as the Flexner-Harris. 
The especial habitat of the disease is the tropics, particularly Japan, the 
Philippines, Porto Rico, etc., where widespread and fatal epidemics 
are common; but sporadic cases occur elsewhere in the tropics and in 
practically the entire temperate zone, and epidemics are by no means 
infrequent, especially in the summer and fall. General insanitary 
conditions, such as may prevail in barracks, jails, asylums, etc., materially 
favor the spread of the infection, which also is one of the notable scourges 
of camp life and frequently numbers more victims than the military 
prowess of the enemy (our own Civil War, the South African War, etc.). 
How the infection is transmitted is not definitely known; the factors are 
believed to be similar to those of typhoid fever. The bacillus may be 
cultivated from the intestinal discharges and the blood, and from the 
intestinal contents and wall after death. In many cases they persist in 
the intestinal tract for a long time after apparent recovery, and may be 
cultivated from the intestinal discharges, either periodically or at all 
times: these cases constitute the so-called " chronic carriers," who are 
responsible for many epidemics. Amoeba coli may be found associated 
with Bacillus dysenterise in some cases. 

Dysentery is rather common also as a terminal event in certain wasting 
and debilitating disorders, and similar symptoms are observed sometimes 
to follow the ingestion of unwholesome food, especially unripe or over- 
ripe fruit, certain preformed poisons, etc. The summer diarrhoeas of 
children also are often due to Bacillus dysenterise infection. 

Pathology. — Two types of the disease may be recognized, the acute 
and the chronic. In acute cases ending fatally within a week, the mucous 
membrane of the large intestine is markedly swollen, cedematous, and 
hyperemic, and covered with blood-stained mucus, the solitary follicles 
are enlarged, foci of hemorrhage are present in the mucosa and sub- 
mucosa, and the superficial layer of the mucosa (in folds, irregular 
patches, or larger areas) is necrotic and may be readily removed. In 
more severe infections the entire wall of the large intestine is very much 
thickened and stiffened (oedema, congestion, and cellular infiltration), 
and the mucosa is grayish black in color — necrotic or gangrenous. 
Even the serous coat may be involved, and sometimes the ileum shows 
more or less well-advanced lesions. The changes in the mucosa consist 
of coagulation necrosis with the exudation of fibrin and polynuclear leuko- 
cytes (pseudomembrane). The submucosa shows hemorrhages, fibrin 
formation, and irregular cellular accumulations (chiefly plasma cells); 
these are believed to be toxic in nature, since they may be present with 
an intact mucosa, and bacteria, as a rule, are not encountered amidst 
t hem. IJlceration does not occur, any loss of tissue resulting being due to 
exfoliation of necrotic mucosa and attached pseudomembrane. Should 



BACILLARY DYSENTERY 147 

the patient not die, the acute lesions may subside or they may become 
chronic. Of the chronic infection, follicular, diphtheritic, and gangren- 
ous forms are sometimes described — which, however, are merely stages 
of the one disorder. -In the milder follicular type there is necrosis and 
ulceration of the solitary follicles, with the gradual extension of the proc- 
esses to the mucosa and submucosa and sometimes the muscular coat — 
whence superficial and often deep ulceration results (doubtless, in part 
at least, attributable to secondary, especially pyococcic, infection). A 
croupous or so-called diphtheritic membrane is present in many cases; it 
is usually irregularly distributed, and associated with more or less ex- 
tensive sloughing, so that a characteristic shaggy appearance is produced. 
In other cases, more or less widespread gangrene occurs. Healing may 
ensue, but it is usually extremely slow, being much retarded by the 
secondary pyococcic invaders; as it occurs, irregular cicatrices develop 
which not only replace the mucous membrane, but, contracting, give 
rise to considerable distortion and even obstruction of the intestines. 
Polypoid outgrowths also are a feature of many chronic cases. The 
specific microorganism may be isolated from the lesions, especially during 
acute exacerbations — which are quite prone to occur. 

Symptoms. — The period of incubation is believed to be, as a rule, 
less than forty-eight hours, and the onset of the disease rather sudden — 
with abdominal distress, frequent bowel movements, and fever (101° to 
102° F.). In other cases the onset seems less sudden, the dysenteric 
symptoms developing out of what appears to be an ordinary diarrhoea. 
In whatever way developing, the bowel is soon rid of fecal matter, and 
although small amounts may still be passed from time to time, the stools 
consist largely, if not exclusively, of mucus admixed with blood and 

; sometimes with pus, and in aggravated cases shreds of necrotic mucous 

! membrane or even larger sloughs of the bowel. The stools are small 

| in amount and very malodorous ; they vary in number from ten to thirty, 
forty, or more in the twenty-four hours; they are usually accompanied 

I and followed by extremely painful and distressing tormina and tenesmus. 

1 The abdomen is distended and often tender along the course of the colon. 
The constant straining may result at first in spasm and later paralysis of 

I the sphincter, and even prolapse of the rectum. Evidences of general in- 
fection are seen in the fever, which may increase to 103° to 104° F. in 
the first few days, headache, occasional vomiting, loss of appetite, coated 
tongue, thirst, scanty albuminous urine, and rather rapid emaciation. 

1 In very severe infections, the rectal tenesmus and efforts at stool may be 
almost constant, the bloody mucous stools may be replaced by more 
serous discharges, abdominal distress and colonic tenderness may become 
extreme, delirium and the typhoid state (toxemia) may supervene, and 
in collapse the patient may die within three or four days. In the majority 
of cases, however, the stools lessen in number in from four to six days, 
the tenesmus subsides, the fever disappears, and the patient begins 
to improve generally, though some blood and mucus may persist for 
several weeks. In some cases improvement is arrested after ten days 



148 BACTERIAL INFECTIONS 

or two weeks, and the general nutrition of the patient begins again 
to fail; he becomes anemic and emaciated, his pulse becomes weak 
and small, his temperature perhaps subnormal, and he passes into 
chronic dysentery. He may have three or four stools in the twenty-four 
hours — partly fecal, partly mucous, and sometimes admixed with 
blood, and acute exacerbations may occur from time to time ; or consti- 
pation may alternate with diarrhoea. Recovery may finally ensue, or 
death may eventuate from exhaustion or some intercurrent infection. 

Complications and Sequels. — Peritonitis sometimes occurs, but it is 
due rather to extension through the wall of the intestine than to per- 
foration; perityphilitis or periproctitis is the most common. Inflam- 
mation of the other serous membranes, arthritis, pylephlebitis, etc., 
have been observed. Anemic oedema, amyloid disease, neuritis (with 
paraplegia and other paralyses), chronic nephritis, pyemia, intestinal 
obstruction, etc., may follow chronic dysentery. 

Diagnosis. — The diagnosis is usually quite apparent from attention 
to the stools. The nature of the infection may be ascertained by re- 
course to the serum agglutination test with the dysentery bacillus (the 
Shiga organism, but especially the Flexner-Harris type in this country); 
by cultivating the organism from the stools; and by the deviation- or 
fixation-of-the-complement test. 

Prognosis. — The prognosis depends, as a rule, upon the severity of 
the infection. The acute forms, especially when occurring in epidemics, 
are very fatal. In milder cases the persistence of blood and mucus 
is unfavorable. As a secondary infection in debilitated subjects, dysen- 
tery often determines the fatal outcome. 

Treatment. — The prophylactic measures advised in connection with 
the infectious diseases (page 29), especially typhoid fever, should be 
carried out, since there is reason to believe that the factors in infection 
are similar to those of typhoid fever. In particular, the stools should 
be rigorously disinfected. 

Rest in bed during the acute stage is essential. The diet must be 
the blandest — milk (peptonized, or diluted with barley water, lime water, 
or Vichy water), albumen water, raw eggs, beef juice, broths, custard, 
milk toast, etc. In subsiding or chronic infections the greatest atten- 
tion also must be paid to the diet, since recurrences are not infrequently 
provoked by dietetic indiscretions. It is wise at the beginning of the 
attack, if there has been little diarrhoea, to clear out the bow T el with blue 
mass, calomel, or castor-oil to which 20 minims (1.25 c.c.) of tincture 
of opium may be added. Following this, one should prescribe so-called 
intestinal antiseptics and astringents, such as: 



]$ — Bismuth subnitrate (or subgallate) 3 drams 12 

Salol 1 dram 4 

Deodorized tincture of opium 2 drams 8 

Chalk mixture, sufficient to make 3 ounces 100 

• s - — Two teaspoonfuls (10 c.c.) every two or three hours, as required. 






0— M. 



TETANUS 149 

Bismuth salicylate, beta-naphthol, resorcin, creasote, zinc sulpho- 
carbolate, and similar drugs are also useful; or one may give mercuric 
bichloride, T ^ grain (0.0006 gram), every two hours. In other cases, 
the following often leads to marked amelioration of the symptoms : 

I^ — Lead acetate 20 grains 1 3 

Powdered opium 5 grains 3 

Camphor 10 grains 65 

Mix and make ten capsules. 

S. — One capsule every two or three hours, as required. 

In some severe cases of undetermined or supposed amoebic nature, 
recourse may be had to the ipecac treatment mentioned under amcebiasis 
(page 177). Irrigation of the bowel is of very great advantage in many 
cases, but the pain and tenesmus are often almost insurmountable 
obstacles to its use in acute cases; but sometimes these may be at least 
partially overcome by a preliminary enema of laudanum (J to 1 dram, 
2 to 4 c.c.) and thin starch water (2 to 4 ounces, 60 to 120 c.c), or a 
cocaine or iodoform suppository. The irrigation should be done by 
means of a fountain syringe and the tube should be inserted high up in 
the sigmoid; a double catheter may be employed, so as to facilitate the 
exit of the fluid; and the fluid should be quite cold or quite hot (110° F.). 
From two to four pints (1 to 2 liters) of any of the following solutions 
may be employed: Silver nitrate, 0.1 to 0.5 per cent.; zinc sulphocar- 
bolate, 0.1 to 0.3 per cent.; lead acetate, 0.1 to 0.3 per cent.; and salicylic 
acid, 0.2 to 0.5 per cent. In chronic cases, in addition to attention to the 
diet, large doses of bismuth, intestinal antiseptics, a lead and opium 
pill, and irrigations, especially with silver nitrate (1 to 5 per cent., fol- 
lowed by injection of sodium chloride solutions), should be tried. In 
some chronic cases rebellious to medical treatment, appendicostomy 
with subsequent irrigation of the colon has been followed by much 
benefit. A satisfactory antidysenteric serum has not yet been produced. 



TETANUS. 

(Lockjaw.) 

Tetanus is an acute, specific, infectious disease caused by Bacillus 
tetani (Nicolaier), and characterized by increased reflexes and tonic 
spasms of the voluntary muscles. 

Etiology. — The tetanus bacillus is widely distributed in nature, being 
found in the intestine of herbivorous animals, in manure, in the soil, 
in dust, in rust, in gun-powder, etc. An essential factor in the etiology 
of the disease is a wound — whence infection occurs; since, although 
two varieties of tetanus are described, the so-called idiopathic and the 
traumatic, careful observation is reducing materially the supposed 
idiopathic cases. These are said to develop after exposure to the 
inclemencies of the weather, especially after sleeping on damp ground, 
but small abrasions cannot be excluded in these cases. In other 



150 BACTERIAL INFECTIONS 

cases, doubtless, insignificant wounds of the nose or the mouth afford 
ready entrance for the tetanus bacillus. The obviously traumatic 
cases follow wounds, especially contused and punctured wounds of the 
hands and feet, but also gun-shot wounds of any part of the body; they 
are not (or were not) infrequent in the newborn (tetanus or trismus 
neonatorum), infection occasioned by filthy dressings occurring by way 
of the umbilicus; and they sometimes occur in puerperal women, infec- 
tion occurring by way of the genital tract. The disease is said to be more 
common in the negro than in the white race, and in the tropics than in 
the temperate zone — doubtless, however, merely in consequence of 
accidental factors. 

The tetanus bacillus, having gained access to a wound, develops and, 
especially when associated with pyogenic cocci, produces a toxin of 
extreme activity (a fractional part of a milligram having been estimated 
to be a fatal dose). This is taken up by the lymphatics of the nerves 
and conveyed to the central nervous system, where it enters into such 
firm combination with the nerve cells that it frequently cannot be dis- 
sociated nor its effects overcome — although a potent antitoxin can be 
produced in the lower animals. The tetanus bacillus may be isolated 
from the wound, and recently has been found also in the lymph nodes 
adjacent to the infected wound. 

Pathology. — Irregular congestions of the central nervous system, 
degeneration of nerve cells, and swelling and oedema of the peripheral 
nerves are encountered, but the lesions are in no way characteristic. 

Symptoms. — The period of incubation is from five to fifteen days, 
as a rule. The shorter the period the more severe the symptoms and 
the more likely death. Generally there are no noteworthy prodromes. 
Preceded sometimes by general malaise, headache, occasionally chilli- 
ness, the disease begins with gradually increasing stiffness and tension of 
the muscles of the jaw and the neck, and difficulty in mastication. In 
a few cases the first manifestations are in the muscles near the site of 
infection. Gradually the tonic spasm involves almost all the voluntary 
muscles of the body: the jaws become locked, immobile; the forehead 
becomes wrinkled, the eyelids partly closed and the eyes staring, and 
the angles of the mouth drawn down and out (risus sardonicus); the 
head becomes retracted; spasm of the spinal muscles causes arching of the 
vertebrae (opisthotonos). The abdominal muscles become rigidly con- 
tracted; sometimes such is the contraction that the body may be arched 
forward (emprosthotonos) or rupture of the muscle may occur. The body 
is rarely arched to the side (pleurosthotonos). The legs and the trunk 
are sometimes extremely rigid (orthotonos), the patient being, as it were, 
held in a vice. The arms, as a rule, are relatively unaffected. Occa- 
sionally strabismus develops. The persistent tonicity of the muscles is 
made worse by paroxysmal exacerbations, which, induced by the slightest 
jar or noise, recur at irregular intervals, last from ten to thirty seconds, 
arc accompanied by profuse perspiration, and occasion the greatest 
agony. The distress is frequently augmented by spasmodic dysphagia, 



TETANUS 151 

and by spasm of the muscles of respiration, of the diaphragm, and of 
the glottis, causing asphyxia which may prove fatal. 

The mind is usually clear, the superficial and the deep reflexes are 
greatly exaggerated, and the patient is often wakeful (but the spasms 
often lessen during sleep). The pulse is rapid (100 to 140). The 
temperature may be normal, but it is usually somewhat elevated; hyper- 
pyrexia is common in fatal cases (108°, 110°, 112° F.), and may even 
increase after death. The urine may be suppressed, or difficulty in 
voiding urine secreted may be experienced. Occasionally slight albu- 
minuria or glycosuria is found. 

Acute and chronic, severe and slight, cases may be distinguished. 
In the acute cases the phenomena develop rapidly and soon become 
intense, paroxysm following paroxysm with rapidity; death usually 
follows within three or four days from exhaustion, asphyxia, or heart 
failure. In more favorable cases the paroxysms become less frequent 
and less severe, and the patient may recover after the lapse of several 
weeks, though exhaustion may last for a long time and eventually prove 



A special form is the cephalic tetanus of Rose, which follows injuries 
to the cranial nerves (especially the face), and is characterized by 
paralysis of the muscles supplied by the facial nerve on the side of the 
injury, and spasm of the masseters and of the muscles of deglutition 
(tetanus hydrophobic us), and sometimes of the muscles of the neck 
and the trunk. 

Diagnosis. — The disease is usually unmistakable. In strychnine 
poisoning, as contrasted with tetanus, there is often a history of the 
ingestion of a supposed poison; the spasms are violent from the beginning, 
but do not begin with trismus, and are marked in the extremities (relative 
freedom of the arms in tetanus); there are intervals of complete relaxa- 
tion (as contrasted with the persistent tonicity of tetanus) ; and strychnine 
may be found in the gastric contents. Tetany is often associated with 
rickets or gastric dilatation; the spasms involve the extremities, especially 
the hands and the feet and the larynx; and Erb's, Chvostek's, and Trous- 
seau's signs may be elicited. In hydrophobia there is a history of the bite 
of a supposedly rabid animal; the spasms involve especially the muscles 
of deglutition and of respiration; there are marked psychic symptoms; 
and there is no lockjaw, no persistent tetanic spasm, and no opisthotonos. 
Hysteria occurs especially in neurotic women; the spasms may begin 
suddenly and last for hours or days ; laughing and crying spells are com- 
mon, especially upon the relaxation of the spasm; and other phenomena 
of hysteria may be elicited. 

Prognosis. — The mortality of acute traumatic tetanus, of puerperal 
tetanus, and of tetanus in the newborn is over 90 per cent. In the sub- 
acute or chronic cases the mortality is not more than 50 per cent. Favor- 
able symptoms are late onset of the symptoms (two weeks or more after 
the injury), more or less restriction of the spasms to the jaw and neck, 
lessening of the paroxysmal exacerbations, and the absence of fever. 



152 BACTERIAL INFECTIONS 

Treatment. — The patient should be kept absolutely quiet -jin a darkened 
and secluded room, free from all irritating noises and solicitous friends. 
The diet must be light and nutritious, and administered in small amounts 
at frequent intervals. Should the patient be unable to swallow, a stomach 
tube may be passed through the nose or mouth (space left by absent 
teeth) and the patient thus fed, or recourse may be had to rectal alimen- 
tation. Inasmuch as the toxin is manufactured in the local wound, 
wisdom suggests its removal; should this be impossible the wound must 
be thoroughly cleansed and antisepticized. 

The tetanus antitoxin has not sustained the early claims made for it, 
not so much, however, because it is impotent as because by the time it 
is generally used the tetanus toxin has already effected such a firm com- 
bination with the nerve cells as to prohibit all efforts at its dissociation. 
It is imperative, therefore, that the antitoxin be administered at the 
earliest possible moment, and in large amounts (2000 to 7000 units) . It 
should be injected into and subcutaneously about the wound, and it 
may also be injected into the nerve trunks leading from the infected 
area, where perhaps it may meet and neutralize the toxin, being thus 
conveyed to the central nervous system. The antitoxin has been 
administered to a fairly large number of persons (mostly children) 
injured with toy pistols (Fourth-of-July celebrations) with a marked 
reduction of the morbidity incidence and the mortality. In view of the 
uncertain results attending the subcutaneous and intravenous injection 
of the antitoxin, its injection beneath the cerebral membranes or directly 
into the brain tissue has been practised — with improved results. This 
seems to me a rather unnecessary and hazardous proceeding, especially 
in view of the fact that the same object can be achieved by injecting it 
into the subarachnoid space by means of lumbar puncture. One should 
first assure himself that he has penetrated the arachnoid membrane, 
by withdrawing a considerable amount of the cerebrospinal fluid, and 
should then inject the antitoxin (30 c.c.) and subsequently more or less 
invert the body so as to insure the thorough mixing of the antitoxin with 
the remaining cerebrospinal fluid. The procedure should be repeated 
in accordance with the exigencies of the case. Meltzer, Miller, and 
others recently have obtained good results from the subarachnoid injec- 
tion of a 25 per cent, solution of magnesium sulphate, of which from 
1 to 2.5 c.c. may be used daily or every second day, depending upon 
the indications. Baccelli speaks highly of the hypodermic use of 
carbolic acid — in 2 per cent, solution, from 3 to 5 grains daily. I 
have thought that I have seen it do good. The spasms are best con- 
trolled by the use of chloroform and morphine, either or both of which 
should be given in sufficient dose. Chloral and the bromides are useful 
adjuvants. Stimulants (alcohol, digitalis, caffeine, etc.) are often called 
for to combat exhaustion and to maintain the failing heart. Cannabis 
indica, calabar bean, belladonna, curare, amyl nitrate, etc., have also been 
recommended. 



CHOLERA 153 

CHOLERA. 

{Asiatic Cholera.) 

Cholera is an acute, specific, infectious, and moderately contagious 
disease caused by Microspira comma (Koch), and characterized by 
vomiting, profuse " rice-water" intestinal discharges, suppression of 
urine, collapse, and frequently death. 

Etiology. — Cholera is endemic in India and has occasionally pre- 
vailed epidemically in Europe and this country. It always follows 
the channels of commercial intercourse (immigrants, pilgrims, shipping, 
etc.), and is in consequence more common in sea-ports than in inland 
towns. Age, sex, and race are of no etiological importance. Persons 
debilitated from any cause, the impoverished, alcoholics, subjects of 
chronic gastro-intestinal catarrh, mental depression, etc., seem especially 
susceptible. Some persons (50 per cent, of the population, Koch) 
are apparently naturally immune. One attack confers a temporary 
immunity. 

Infection is spread especially by water — that used for drinking pur- 
poses, that used in preparing foods, such as milk, lettuce, and other 
foods eaten uncooked, and that used in domestic washings, etc. Infec- 
tion, thus, is acquired by ingestion. Flies seem to be active agents 
in disseminating the infection. The disease is only slightly contagious. 
Infection is not transmitted by the air (the comma bacilli die soon when 
dried), but some persons have become infected from handling infected bed- 
linen, dishes, etc., and several cases of laboratory infection have been 
observed. 

Pathology. — In consequence of the great loss of fluids through vomit- 
ing and diarrhoea, the body after death is shrunken and withered. Post- 
mortem rigidity comes on soon, is extreme (occasioning distortion of 
the body), and persists for a long time. Postmortem twitchings of the 
muscles (causing movements of the dead body) and even elevation 
of the temperature have been observed. The blood is thick and dark- 
colored, and the organs, as a rule, are unusually free of blood and dry. 
The important lesions are in the intestinal tract. The peritoneum 
is dry, though sometimes curiously sticky, and the coils of intestine 
are shrunken and thin. The intestinal contents resemble the "rice- 
water" discharges. The mucous membrane at first is swollen and con- 
gested and covered with an excessive secretion of mucus; later the 
lymphoid follicles become swollen, and may reveal irregular foci of 
congestion, occasionally of hemorrhage; the epithelium desquamates 
and may even be shed in rather large masses, leaving the submucosa 
denuded. Occasionally extensive necrosis and ulceration, rarely 
perforation, may be observed. The mesenteric lymph nodes are often 
swollen; the spleen is not enlarged. The other organs manifest the lesions 
common to most toxemias, modified, however, by the unusual loss of 
fluids. The comma bacilli may be found in the contents of the intestine 



154 BACTERIAL INFECTIONS 

and in the mucous membrane; in protracted cases they may be found 
in the wall of the intestine and even in the mesenteric lymph nodes. 

Symptoms. — The period of incubation is from one to three days. 
In some cases a premonitory stage may be distinguished — in which 
there may be some epigastric distress, diarrhoea, and weakness. Often, 
however, the onset of the disease is abrupt, coming on apparently in 
the midst of perfect health, with chilliness, profuse diarrhoea, and extreme 
prostration or collapse (stage of collapse). The stools are at first fecal 
in character, but they soon become grayish, alkaline, watery, odorless, 
and contain flakes of mucus, epithelial cells, and granular debris (" rice- 
water" stools), occasionally blood, and they usually reveal the comma 
bacillus in pure culture. There may be thirty or more stools within the 
first twenty-four hours. Usually they are passed painlessly, but occasion- 
ally there is complaint of abdominal pain and tenesmus. Vomiting soon 
comes on and becomes persistent, thirst is extreme and very distressing, 
painful cramps develop in the muscles of the abdomen and legs, prostra- 
tion and collapse become more marked, and the toxemia and concen- 
tration of the blood increasing, the patient passes into the algid stage. 
The cutaneous temperature is much below normal and the skin feels 
cold and clammy, though the internal (rectal) temperature may be 103° 
to 105° F. ; the extremities are cyanotic, the face grayish, ashen, or 
exhibits a slight cyanotic tint; the features are pinched, the eyes 
and cheeks sunken, and the skin in general withered and wrinkled. 
The pulse becomes weak, the heart sounds indistinct, the blood pressure 
low, the voice hoarse and weak, the breathing labored and superficial 
(asphyxic stage), and the urine much reduced in amount, and contains 
albumin, casts, and erythrocytes; not infrequently it is totally sup- 
pressed. Consciousness is often maintained throughout, but the patient 
may pass into coma, with or without delirium, and die — sometimes 
within the first twenty-four or forty-eight hours. 

In some cases, however, the patient improves and the stage of reaction 
(tepid stage) sets in. The vomiting ceases, the intestinal discharges 
lessen and become more fecal in character, the pulse becomes stronger, 
the respirations easier, slower, and deeper, and the surface temperature 
normal; not infrequently the skin is covered with sweat, and the func- 
tions of the kidneys are gradually restored, though albuminuria per- 
sists for some time. In favorable cases the patient continues to improve, 
and convalescence is established at the end of ten days or two weeks. 
Not infrequently, however, diarrhoea recurs at the end of two or three 
days, the patient passes rapidly again into the algid stage, and soon 
dies. In other cases so-called typhoid cholera develops; the patient 
becomes delirious and often feverish, and the pulse rapid and weak; 
the urine is again suppressed, coma and perhaps convulsions super- 
vene, and death usually ensues, though recovery has been observed. 

Varieties. — Some attacks are so mild that the patient is slightly, 
if at all, indisposed, complaining only of a little diarrhoea; indeed, 
during epidemics the cholera bacillus has been found in the stools 



CHOLERA 155 

of presumably healthy persons. The term cholerine has been applied 
to cases, resembling, if not identical with, cholera nostras (due to bacteria 
other than Microspira comma), in which there is profuse diarrhoea, 
possibly vomiting, but only moderate collapse, and rather quick recovery. 
In other cases the patient is overwhelmed with the intoxication and 
dies within a few hours, in coma, even before the onset of diarrhoea 
(cholera sicca). As a rule, the symptoms are directly proportional to 
the loss of fluid and the salts of the blood. 

Complications and Sequels.— The most common are: protracted con- 
valescence and anemia, nephritis, uremia, cutaneous rashes (roseola, 
erythema, urticaria), pneumonia, arthritis, parotitis, chronic enteritis 
and colitis, gangrene, especially of the toes, etc. 

Diagnosis. — In the presence of an epidemic it may be difficult or 
impossible to distinguish between cholera asiatica and cholera nostras, 
except by a bacteriological examination of the intestinal discharges. 
The "rice-water" discharges of the early days of true cholera usually 
reveal the cholera bacillus in pure culture; later certain contaminating 
bacteria are usually encountered; while still later the cholera bacillus 
may be detected only with difficulty. The agglutination test may prove 
of service. Certain forms of food-poisoning, of fungus-poisoning, and 
of metallic poisonings (arsenic, antimony, and corrosive sublimate) may 
simulate cholera, but the associated phenomena usually preclude diag- 
nostic error. 

Prognosis.— The mortality varies from 50 to 80 per cent, in different 
epidemics, and is in direct ratio to the severity of the infection. Most 
deaths occur during the algid stage. 

Treatment. — Prophylactic measures are of the greatest importance, and 
the strictest sanitary measures must be enforced (page 29). As in the 
past, rigid quarantine will prevent the introduction of the disease into 
this country. Haffkine's preventive inoculations have proved of some 
service, and seem to merit continued trial. During the prevalence of an 
epidemic all drinking water and milk should be boiled, and no uncooked 
food should be eaten. Dilute sulphuric acid, 20 minims (1.25 c.c), in a 
pint (500 c.c.) of water, three times daily, is believed to be a serviceable 
prophylactic, since dilute acids kill the vibrios. All diarrhceic attacks of 
whatsoever nature must be promptly treated — by preliminary cleansing 
of the bowel (castor oil), and by astringents, such as bismuth, lead acetate, 
aromatic sulphuric acid, and opium. 

When the disease has developed the patient must be kept at rest in 
bed in a warm room (to help maintain the bodily heat), and upon the 
development of the algid stage, he should be surrounded by hot bottles, 
etc. Morphine or Dover's powder is useful in the early stage in allaying 
the pain; hot applications to the abdomen (mustard plaster, spice 
poultice, turpentine stupe, etc.) are grateful. In the event of vomiting, 
small doses of calomel should be administered; most other remedies, 
such as cocaine, are useless. Efforts may be made to restrain the diar- 
rhoea (aromatic sulphuric acid and astringents), but unfortunately our 



156 BACTERIAL INFECTIONS 

best directed efforts are usually in vain. Enteroclysis with hot physiologi- 
cal saline solution, to which tannic acid (1 per cent.) and tincture of opium 
have been added, may be tried. Intestinal antiseptics seem to be indi- 
cated on theoretical grounds, and good results have been claimed for 
salol; naphthalene, resorcin, etc., may also be tried. The most effi- 
cacious treatment appears to be that recommended by Rogers and 
others — the intravenous injection of hypertonic (1.35 per cent.) sodium 
chloride solution: four drams (16 grams) to a quart (liter) of water. 
Of this two liters should be injected at a time, and repeated as occasion 
may warrant. Rogers adds to the first and second injection fluid, cal- 
cium chloride, 6 grains (0.4 gram) to the quart (liter), to overcome the 
low coagulability of the blood. The fluid may also be injected into the 
peritoneal cavity; and this may be augmented by hypodermoclysis and 
hot enteroclysis (107° to 110° R). If the patient is not vomiting, fluid 
should also be given by the mouth. Strychnine, whiskey, brandy, cam- 
phor, hot coffee or tea, and more diffusible and rapidly acting stimu- 
lants, such as aromatic spirit of ammonium, and compound spirit of 
ether, etc., are also indicated in most cases. The uremic manifestations, 
which are likely to develop during the reaction stage, are associated 
with low blood pressure (80 to 90 mm. Hg.), and are to be combated 
By the hypodermic or intravenous administration of adrenalin and digi- 
talis. Should the patient survive the algid stage, he must be fed care- 
fully with bland liquid foods, small amounts at stated intervals, and 
every precaution must be observed not to provoke diarrhoea. 



PLAGUE. 

(Bubonic Plague; Bubonic Pest; Oriental Plague.) 

Plague is an acute, specific, infectious, and slightly contagious dis- 
ease caused by Bacillus pestis (Kitasato), and characterized by fever, 
inflammation of the lymph nodes (buboes), of the lungs, and of the 
cellulo-cutaneous tissues, and a general bacteremia. 

Etiology. — The plague has prevailed epidemically since the early 
days of the Christian era, and has been answerable for great loss of life 
—notably during the fourteenth century, when a fourth of the population 
is said to have succumbed, and in 1665, when 70,000 persons died in 
London. Following a period of comparative quiescence, the plague 
recently has appeared in different parts of the world — having been dis- 
seminated from India, where it has been endemic. It has been carried 
to many ports of Europe, Africa, Australia, and this country, and small, 
local epidemics in and about the seaports have developed; but proper 
sanitary measures have served to prevent serious outbreaks. Age, 
sex, race are without etiological significance. The disease is especially 
common among the poor and those living under unhygienic conditions. 
It prevails especially during the warm seasons, but also during the colder. 
One attack confers partial immunity. 



PLAGUE 157 

The exciting cause of the disease is Bacillus pestis, which may be found 
in the blood, lymph nodes, secretions, and viscera of patients and of 
subjects dead of the disease. The disease is only slightly contagious — 
contagion being a factor in less than 3 per cent, of the cases (Plague 
Commission). The infection is spread largely through the medium of 
rats; an epidemic among rats commonly precedes infection in man in 
new localities. The infection is transmitted from rat to rat, and from 
rat to man, by means of rat fleas — which may be carried from place to 
place by human subjects on their person or in their baggage, etc. Re- 
cently in California the ground squirrel has been found to be infected, 
and doubtless propagates the disease. Infection is acquired in the great 
majority of cases by means of the bites of infected rat fleas, but it 
may also be acquired by direct inoculation into a wound or abrasion 
(handling of infected material, laboratory investigations, etc.), by inhala- 
tion (pneumonic type), and perhaps by ingestion (contaminated food 
and drink — probably rare) . 

Pathology. — The lesions vary somewhat with the type of the infection, 
but in all there is a general plague bacillemia; the lymph nodes are 
swollen, hyperemic, later hemorrhagic, purulent, and more or less difflu- 
ent; the lymphatic vessels are inflamed, and about both there is more or 
less oedema. Hemorrhagic foci are present in the skin, the serous mem- 
branes (pleura, pericardium, peritoneum), and in the mucous membrane 
of the gastro-intestinal tract. The liver and kidneys show cloudy swell- 
ing and often hemorrhages, and the spleen is much enlarged and softened. 
In the pneumonic type there is swelling and congestion of the bronchial 
mucous membrane, and foci of bronchopneumonia. 

Symptoms. — The period of incubation is usually two or three days, 
although it may be as long as five or seven. Several varieties of the dis- 
ease may be distinguished : bubonic plague, pneumonic plague, cellulo- 
cutaneous plague, septicemia plague, and pestis minor. 

Bubonic or glandular plague is the most common (80 per cent, of 
the cases). In most cases, following several days of irregular prodromes, 
such as malaise, chilliness, and headache, the disease develops suddenly 
with fever (103° to 104° F.), increased headache, anxiety, restlessness, 
and general neuromuscular pains or aching. The pulse becomes rapid 
(a valuable diagnostic sign), the respirations increased in frequency, 
the face and the conjunctiva injected, the tongue coated, the bowels 
constipated (though diarrhoea may supervene), and the patient becomes 
greatly depressed. Usually there is a polynuclear leukocytosis. In 
severe cases the patient may become collapsed, the urine scanty, 
almost suppressed, delirium may supervene, and in uremic coma 
or convulsions the patient may die, even within the first twenty-four 
hours (pestis siderans). In three-fourths of the cases, however, at 
the end of twenty-four or forty-eight hours (rarely later), the charac- 
teristic lymph-node swellings (buboes) develop, usually on one side, some- 
times on both, and most frequently in the groin, less commonly in 
the axilla, the neck, or internally. The swellings vary much in size, 



158 BACTERIAL INFECTIONS 

up to that of an orange, and they are tender and painful. Soon peri- 
glandular swelling and oedema develop to such a degree as to obscure 
or obliterate the outlines of swollen lymph nodes. By the second or third 
day the fever has reached its maximum; it often drops somewhat on the 
third or fourth day, then rises (sometimes to 108° F.), and in favorable 
cases by the seventh or the eighth day begins to fall by lysis and gradually 
reaches the normal. The glandular swellings may undergo resolution 
or suppuration (commonly a good sign); in some cases, however, more 
or less extensive sphacelation and generalized furunculosis occur. In 
other cases concurrent with the development of the buboes hemorrhages 
into the skin occur (plague spots, "fatal tokens" — whence the designa- 
tion " black death"). Hemorrhages from the mucous membranes are also 
encountered. In the event of suppuration, the purulent discharge may 
rapidly abate, or the sinuses may become indolent and the patient event- 
ually die of exhaustion, amyloid disease, or secondary infections. The 
mortality is about 75 per cent. 

Pneumonic plague is characterized by the development of patches of 
bronchopneumonia. The disease begins with the ordinary manifesta- 
tions of pneumococcic infection of the lung (pneumonia), for which it 
is frequently mistaken. The fever is high and may become intermittent; 
the patient becomes delirious, prostrated, and much sicker than the physi- 
cal signs in the lung indicate. The sputum is thin, serosanguineous (not 
rusty), and contains plague bacilli in abundance. Death occurs usually 
before the fifth day. The mortality is very high — 96 to 100 per cent. 

Cellulocutaneous plague is characterized by inflammation and necrosis 
of the skin and subcutaneous tissues, and is often associated with in- 
volvement of the lymph nodes. The local lesions usually spread from 
day to day until a very large area may become involved, whereupon in 
favorable cases the process may become circumscribed by a well devel- 
oped line of demarcation, and in the course of time a spachelus may be 
discharged. The general manifestations are those mentioned under 
bubonic plague. 

Septicemic plague is a severe plague bacteremia — the general lym- 
phatic system and the blood being overrun with plague bacilli. The fever 
is usually moderate only (100° to 102° F.), the depression extreme, and 
hemorrhages common. The patient usually dies before the lymph nodes 
become palpably enlarged. The mortality is over 95 per cent. 

Pestis minor, pestis ambulans, is a mild form of the disease, character- 
ized by mild fever of several days' duration, swelling and possibly 
suppuration of the lymph nodes, but usually with general symptoms 
so slight as not to necessitate the patient's taking to bed. The patients, 
however, are infectious, and may give rise to widespread dispersion of 
the disease. 

Complications and Sequels. — Complications and sequels are rather 
common. Suppurative disorders of the eye and of the ear (leading to 
loss of sight and of hearing), irritability and rapid action of the heart, 



GLAXDERS 159 

divers nervous disorders and paralyses, and general asthenia are among 
the more common. 

Diagnosis. — During an epidemic the disease is readily recognized. 
In case of doubt, fluid obtained from a bubo (by a sterile hypodermic 
needle), the blood, or the sputum should be examined for the plague 
bacillus; and recourse may be had to the agglutination test. Cultures 
and animal inoculations should be undertaken in the suspicious cases in 
the absence of an epidemic. 

Prognosis. — The prognosis is bad; the mortality varies with the type 
of the infection from 50 to 100 per cent. 

Treatment. — Prophylactic measures of the strictest sort should be 
rigidly carried out. The patient should be isolated, all utensils and 
the body linen should be disinfected or destroyed, rats and similar 
animals should be killed and their carcasses burned (as well as dead 
bodies); attendants should observe all sanitary precautions (page 29), 
and should wear close-fitting undergarments so as to prevent as far as 
possible bites of fleas. Haffkine's prophylactic injections, or "vaccine," 
consisting of gradually increasing doses of heat-killed bacilli, seem to 
confer more or less immunity for from six to eighteen months, especially 
if a second injection is made about a month after the first. This is 
true also of Lustig's preventive inoculations. At all events, the measure 
merits continued trial. 

The treatment of the developed disease is purely symptomatic : hydro- 
therapy for the headache, delirium, and other nervous symptoms; mor- 
phine for the neuromuscular pains and general restlessness ; and stimulants 
(strychnine, camphor, ether, whiskey, hypodermoclysis, adrenalin chlo- 
ride, etc.) for the depression and collapse. An ice-bag, or belladonna oint- 
ment, or glycerin and belladona, or evaporating lotions will diminish the 
pain of the buboes — which, when suppuration has occurred, should be 
incised. Cantlie recommends early purgation with calomel and salines, 
and free stimulation. The evidence for or against Yersin's and Roux's 
antitoxic serum is not yet conclusive, although some good results have 
been reported. 

GLANDERS. 

(Farcy; Malleus Humidus.) 

Glanders is a specific infectious and highly contagious disease of horses 
caused by Bacillus mallei (Loeffler-Schutz), and communicable to man; it 
characterized by the development of a granuloma that ultimately under- 
goes softening, and by general septicemia. 

Etiology. — Glanders is preeminently a disease of horses, but occurs 
sometimes in asses and mules, and is rarely transmitted to men. Infec- 
tion is transmitted directly to men, and is acquired through the medium 
of a wound or abrasion of the skin or the oral or nasal mucous mem- 
brane; but the ingestion of infected meat may also transmit the disease. 

Pathology. — Glanders is one of the infectious granulomas, and consists 
of foci of epitheloid cells, giant cells, small round cells, and the specific 



160 BACTERIAL INFECTIONS 

bacillus; these foci tend to undergo softening and form ulcers or abscesses. 
Two forms are recognized: (1) Glanders, in which the lesions develop 
in the respiratory mucous membrane, especially the nose, and where 
by breaking down they result in the formation of ulcers; and (2) farcy, 
in which the lesions develop in the subcutaneous tissues, especially the 
lymphatic vessels and nodes, and where by breaking down they result 
in the formation of abscesses which may discharge through sinuses. 
Both forms are commonly associated; either may antedate the other. 
Furthermore, a bacteremia may ensue, and lesions may be found in any 
of the internal organs — the lungs (bronchopneumonia), the liver, the 
spleen, the kidneys, the brain, the muscles, etc. ; abscesses are then com- 
mon, as well as hemorrhages into the serous and the mucous membranes. 

Symptoms. — The period of incubation is from three to seven days, 
rarely as long as three weeks. Acute and chronic forms may be dis- 
tinguished. 

In acute glanders the onset is abrupt, and is characterized by fever, 
chilliness, headache, neuromuscular pains in the limbs and joints, and 
the local lesions — swelling and congestion of the nose, which is painful 
and tender and discharges a sanious purulent fluid. Examination re- 
veals considerable nodular swelling of the nasal mucous membrane, and 
in the course of several days more or less extensive ulceration, which 
may progress to necrosis of the bone. Lymphangitis is marked and 
the adjacent lymph nodes are swollen and tender. An eruption, at 
first papular, but soon becoming pustular, and often leading to ulcera- 
tion, occurs on the face, about the joints, and sometimes on the trunk; 
it has been mistaken for smallpox. Pneumonia, arthritis, and other 
evidences of bacteremia usually develop, and the patient dies within 
ten days. 

Chronic glanders resembles and is usually mistaken for chronic coryza. 
It is likely to escape diagnosis for some time, unless the nodular swelling 
and ulceration attract the attention of an observing physician. It may 
last for months, and the patient may eventually recover. 

Acute farcy, the result of cutaneous infection, resembles ordinary 
pyococcic infections, or septicemia. The site of the inoculation often 
presents phlegmonous inflammation, the lymphatic vessels become 
inflamed and thickened, and along their course nodular swellings (so- 
called farcy buds) develop, and usually go on to suppuration. Swelling 
and suppuration of the lymph nodes, septic arthritis, disseminated 
abscesses, in short the manifestations of pyemia, ensue, and the patient 
usually dies within two weeks. The nose is not involved and the cuta- 
neous rash of ordinary glanders is not present. 

Chronic farcy presents the local lesions of acute farcy but with 
little reaction, and without the severe general manifestations. The 
farcy buds often soften and form abscesses, and ultimately deep, more 
or less indolent ulcers. The disease may go on for years, but finally 
death results from exhaustion or acute pyemic glanders. 



I 



ANTHRAX 161 

Diagnosis. — Acute glanders and farcy are usually readily recognized, 
but the chronic forms often escape detection; in both, the occupation 
of the patient may afford the first clue. In suspected cases some of the 
discharge should be examined for Bacillus mallei. Some of it may be 
injected into the peritoneal cavity of a male guinea-pig, the testicles of 
which, in the event of glanders, at the end of two days, become swollen 
and soon suppurate, and in the course of two weeks the animal dies 
of generalized nodular glanders (Strauss' test). The mallein reaction 
(similar to the tuberculin reaction) is also of diagnostic value in suspected 
cases. In acute cases the infecting bacillus may be cultivated from the 
blood. 

Prognosis. — The prognosis is bad. 

Treatment. — Treatment in the acute cases is usually unavailing, but 
supportive measures should be employed. In the more chronic cases sur- 
gical measures are indicated. Potassium iodide internally and mercury 
by inunction are said to have been of much service in some cases. Mal- 
lein has not yet proved of much value as a therapeutic remedy. Some 
encouraging results following the use of bacterial vaccines have recently 
been reported. 

ANTHRAX. 

(Malignant Pustule; Anthrax, or Mycosis Intestinalis; Anthrax, or Mycosis Pulmo- 
nalis; Splenic Fever; Wool-sorter's Disease; Rag-picker's Disease; Charbon.) 

V 

Anthrax is an acute, specific, infectious disease caused by Bacillus 
anthracis (Pollender-Davaine) , and characterized by local oedema and 
inflammation, and often by bacteremia. 

Etiology. — Anthrax is a widespread disease of the lower animals — 
most common among the herbivora, less common among the omnivora, 
and least common among the carnivora. It frequently leads to extreme 
devastation of herds of cattle and of sheep, especially in Russia, Siberia, 
and certain parts of Europe — where it is much more frequent than in 
this country. Infection in animals is acquired by direct inoculation 
— through the bites and stings of infected insects, and through feed- 
ing upon infected grain (infected by the feces of diseased animals, for 
instance), and upon the carcasses of animals dead of the disease. Infec- 
tion may be transmitted to man directly through the bites and stings 
of infected insects (flies, mosquitoes, etc.), through the secretions of 
infected animals, through handling infected hides, hair, or wool, or 
through the ingestion of infected food (milk, butter, meat, sausage, 
etc.). Infection is acquired through a cutaneous wound, through the 
respiratory tract (inhaling infected dust) , or through the gastro-intestinal 
tract. The disease is most common among stablemen, butchers, tanners, 
wool-sorters, rag-pickers, hair-cleaners, brush-makers, etc. Most of the 
cases in this country result from handling imported hides, hair, and wool. 
Either the bacilli or their spores may transmit the infection. One attack 
of the disease confers a partial immunity. 
U 



162 BACTERIAL INFECTIONS 

Pathology. — The lesions in man vary, depending upon the mode of 
infection; cutaneous, respiratory, and gastro-intestinal forms may be 
recognized, but in many cases the lesions are widespread. Cutaneous 
infection occurs most frequently on exposed surfaces (the hand, arm, 
face, neck), and is characterized by the development of the so-called 
malignant pustule (which, however, is a misnomer, since the lesion is in 
no way related to ordinary pyococcic pustules). Preceded usually by 
itching, a papule develops at the site of inoculation; this soon becomes 
a vesicle, filled with a clear, more commonly a sanious, fluid, and 
surrounded by a wide area of inflammatory oedema and induration. 
By the end of thirty-six hours the vesicle has dried and a blackish 
eschar has formed; about this there may be a series of vesicles. The 
inflammatory phenomena spread along the lymphatics and give rise to 
lymphangitis, lymphadenitis (and sometimes phlebitis), and to the 
most extreme and widespread oedema. I have seen a small lesion of 
the chin give rise to extreme oedema of the face, neck, arm, and chest. 
Respiratory infection results in severe bronchitis, bronchopneumonia, 
pleuritis, swelling of the bronchial lymph nodes, and marked oedema of 
the mediastinal tissues and sometimes of the neck. Intestinal infection 
results in the development in the mucosa of the small intestine, the 
stomach, rarely the large intestine, of small foci of inflammatory oedema 
and hemorrhage progressing to central necroses, and swelling of the 
mesenteric lymph nodes. Secondary intestinal infection is common in 
the other forms of the disease. In most cases bacteremia develops at the 
end of forty-eight hours. In fatal cases the spleen is enlarged, softened, 
and hemorrhagic, and the ordinary manifestations of toxemia (paren- 
chymatous degeneration, etc.), as well as small hemorrhages, are en- 
countered in the different organs. 

Symptoms. — The period of incubation in cutaneous infections is from 
three to six days, at the end of which time, attended by chill or chilliness, 
fever (102° to 103° F.), headache, malaise, the above-described "malignant 
pustule" develops. Despite the extensive swelling, pain is rarely a con- 
spicuous symptom. The fever often lasts only two or three days, after 
which the temperature may become normal. In unfavorable cases 
symptoms of intestinal infection (vomiting, diarrhoea, etc.), and cerebral 
symptoms, such as delirium, and coma, develop, the pulse becomes 
rapid and weak, profuse sweats ensue, and the patient may die in less 
than a week. In more favorable cases the eschar is separated and 
cicatrization proceeds, the swelling subsides, and the patient eventually 
recovers. All of the three patients that I have seen recovered. 

Malignant anthrax oedema is the name given to a condition differing 
from the foregoing in the absence of a local lesion. The oedema is 
secondary to the general infection, involves the face, head, and some- 
times the arms, and is often so extreme that gangrene results, and the 
patient usually dies. 

In pulmonary anthrax the usual manifestations of severe bronchitis 
and of bronchopneumonia develop — chill, high fever (103° F.), cyanosis, 



ANTHRAX 163 

cough, expectoration (often hemorrhagic and containing the anthrax 
bacillus), prostration, profuse sweats, and collapse. Crackling rales and 
harsh bronchovesicular breathing, sometimes scattered foci of dulness 
(due sometimes to patches of solidification and sometimes to enlarged 
lymph nodes), and bronchial breathing may be detected. So severe is the 
infection in some cases that the patient succumbs within twenty-four to 
forty-eight hours under manifestations of profound intoxication. 

In intestinal anthrax the symptoms usually resemble severe poisonings 
— sudden onset, with chill or chilliness, fever, nausea, vomiting, head- 
ache, pains in the back and legs; later diarrhoea, hematemesis, and 
sometimes blood (and the anthrax bacillus) in the stools, cutaneous 
and mucous membrane petechia, and symptoms of toxemia, such as 
coma, etc., may ensue. Death usually results in from two to five days. 
Intestinal symptoms are common in all forms of the infection. 

Coma and delirium are not infrequent in all forms of the infection, and 
are attributable in most cases to toxemia, but in some fatal cases an un- 
usual infection of the cerebral vessels with the anthrax bacillus has been 
encountered. On the other hand, in quite a few cases the mind is clear 
through the disease. 

Diagnosis. — The cutaneous lesions are quite characteristic and scarcely 
to be mistaken for anything else. From the ordinary carbuncle they may 
be distinguished by the absence of pus and of the slough (so-called core). 
The diagnosis may be confirmed by examining some of the fluid for the 
anthrax bacillus, or injecting it into a guinea-pig or a mouse, which, 
in the event of anthrax, succumbs in a few days to anthrax bacteremia. 
The occupation of the patient may afford the first clue as to the real 
nature of the disease in internal infections (respiratory and intestinal). 

Prognosis. — The prognosis depends upon the severity of the infection. 
The mortality in cutaneous infections about the face is about 25 per cent. ; 
in those about the hand, 10 per cent.; in internal infections, about 90 
per cent. 

Treatment. — Preventive inoculation of animals (Pasteur) with an 
organism of reduced virulence has been practised in certain parts of the 
world with asserted good results. Serum therapy as yet affords us no 
specific in the treatment of the developed disease, although some good 
results have followed the use of Sclavo's serum. In cutaneous infec- 
tions the local lesion should be destroyed with the cautery or excised; the 
wound then should be cauterized with carbolic acid, and treated with 
antiseptic dressings (carbolic acid and mercuric bichloride.) Injections 
into the advancing oedema of carbolic acid (2 per cent.) or of mercuric 
bichloride (1 to 4000) may be of service. Large doses of quinine in- 
ternally have seemed of value in some cases. Stimulants and good food 
are required in all cases. 



164 BACTERIAL INFECTIONS 



MALTA FEVER. 

(Mediterranean Fever; Gibraltar Fever; Rock Fever; Neapolitan Fever; 
Undulant Fever.) 

Malta fever is a subacute or chronic, specific, infectious, and non- 
contagious disease caused by Micrococcus melitensis (Bruce), and 
characterized by peculiar undulatory febrile attacks, profuse sweats, 
swelling of the joints, enlargement of the spleen, and a specific serum 
reaction. 

Etiology. — Malta fever is endemic in the Island of Malta, and in the 
other islands and along the shores of the Mediterranean Sea; and it 
has been observed in China, India, Porto Rico, the Philippines, and 
the United States (imported cases). It is not unlikely that certain of 
the ill-understood fevers of the tropics, especially of Central and South 
America, may ultimately be determined to be of similar nature. The 
disease occurs at all periods of life, but is especially frequent between 
the sixth and the thirtieth year. Sex is devoid of etiological influence. 
The development of the disease seems to be favored by dry weather, 
whence it is most common during June, July, and August. 

The specific cause of the disease is Micrococcus melitensis. In Malta 
the British Army surgeons seem definitely to have proved that the infec- 
tion is derived from the goat; 10 to 15 per cent, of these animals have 
the micrococcus in their milk, and their blood serum gives a positive 
agglutination test. With this infected milk the disease was transmitted 
to monkeys; and stopping the use of the milk remarkably reduced the 
disease among the British troops. Whether the disease may be other- 
wise spread, for instance, by other food or drink, by the air, by the bites 
of insects (mosquitoes, as has been suggested), by fomites, etc., and 
whether it may be acquired by inhalation and direct inoculation (or 
through the conjunctiva, as in Strong's case), as well as by ingestion, 
have not yet been definitely determined. One attack of the disease 
confers a more or less permanent immunity. 

Pathology. — The conspicuous lesions consist of enlargement of the 
spleen, which is hyperemic, soft, and almost, if not quite, diffluent, 
and contains an excess of lymphoid cells; hyperemia of the gastro- 
intestinal tract (occasionally progressing to inflammation and ulcera- 
tion), of the liver, of the kidneys (sometimes progressing to glomerulo- 
nephritis), and sometimes of the meninges. The spleen contains large 
numbers of the specific micrococcus, which may be cultivated without 
difficulty. 

Symptoms. — The period of incubation varies from three to twenty 
days. The onset is gradual and marked by lassitude, malaise, head- 
ache, neuromuscular pains in the limbs, anorexia, and fever, which 
increases day by day, in a more or less well-marked "step-ladder" 
fashion, until at the end of a week or ten days it reaches 103° or 



MALTA FEVER 165 

104° F., in the evening. The morning remissions of the fever are often 
attended by profuse perspiration. As the disease progresses the head- 
ache may become severe; the liver and spleen are found enlarged and 
tender; symptoms of bronchial and of intestinal catarrh may supervene 
(though constipation rather than diarrhoea is the rule); divers joints 
may become swollen, tender, and painful; and the patient usually 
emaciates. At the end of three weeks (or sooner) the fever gradually 
subsides, the other symptoms abate, and the patient apparently enters 
upon a convalescence. At the end of two or three days of apyrexia, 
however, the fever and the other manifestations gradually return, and 
the patient is in a relapse. A series of such relapses, with pyrexial periods 
varying from one to three weeks and separated by periods of apyrexia 
of from one to three days duration, may prolong the disease into months 
— even a year or more. The long-continued fever, often with remis- 
sions so great as to simulate malaria, and the profuse sweats, lead 
usually to marked loss of strength and flesh. 

As a rule, in from seventy to ninety days, convalescence ensues, 
but it may be unusually slow and protracted (six to twelve months), 
and is not infrequently complicated by arthritis, inflammation of fibrous 
structures, neuralgias, orchitis, etc. Death may occur, in scarcely 
more than 2 per cent, of the cases, from exhaustion or an intercurrent 
disorder. 

Several types of the disease are recognized. The term undulatory 
is usually applied to the common form. Occasionally the onset is 
rather sudden, and death may occur within ten days — acute or malig- 
nant type. In other cases the constitutional symptoms are slight, 
consisting only of slight evening fever, malaise, and progressive emacia- 
tion, though more severe symptoms may develop at any time — so-called 
intermittent type. 

Diagnosis.— Malta fever must be distinguished from typhoid fever 
and from malaria. Malaria is readily excluded by the absence of the 
malarial parasite from the blood and the non-response to quinine. Most 
cases, at least in regions remote from the Mediterranean, are mistaken 
at the beginning for typhoid fever, but the absence of many of the 
characteristic symptoms of typhoid fever should be deemed significant. 
The diagnosis is rendered certain by the absence of the Gruber-Widal 
serum reaction with Bacillus typhosus and its presence with Micro- 
coccus melitensis (in some cases as early as the fourth day of the fever). 
The peculiar character of the fever also is quite characteristic, even in 
the absence of the specific serum reaction. The micrococcus in some 
cases may be cultivated from the blood. 

Prognosis. — The duration of the disease is long, but the mortality 
is low — not more than 2 per cent. 

Treatment. — Treatment is purely symptomatic, since an efficient 
serum- or vaccine-therapy has not yet been produced. Hydrotherapy 
and the general measures suitable in typhoid fever are indicated. 



160 BACTERIAL INFECTIONS 

During the periods of pyrexia it is wise to adhere to the diet recom- 
mended in typhoid fever. Drugs, so far as known, seem to have no 
influence on the course of the disease. Convalescence is promoted by 
tonics, change of climate, or a sea voyage. 



LEPROSY. 

Leprosy is a chronic, specific, infectious disease caused by Bacillus 
leprae (Hansen), and characterized by granulomas involving the 
skin, £he mucous membranes, the nerves, the lymphatics, and the 
viscera. 

Etiology. — Leprosy is known to have prevailed centuries before the 
Christian era. At present it is found in all parts of the world, but is 
endemic in India, China, Japan, and other parts of Asia, Africa, Russia, 
Persia, Norway, Sweden, Spain, Portugal, Central and South America, 
the West Indies, Mexico, Iceland, Canada, Australia, the Sandwich 
Islands, etc., and in our own United States, especially Louisiana and 
other southwestern States. From time to time isolated cases have 
been observed in many, if not all, the States, but most of the cases have 
been imported. 

The exciting cause of the disease is Bacillus leprae, which is found 
in leprous lesions, in the secretions therefrom, and in the saliva, and 
oral and nasal discharges in the event of lesions about the nose and 
mouth. The disease is not markedly contagious, since prolonged 
and rather intimate personal contact seems necessary for infection; 
but that the disease may be spread by fomites cannot be denied. It 
has been suggested that fleas, lice, bed-bugs, and the itch parasite 
are the active agents in transmitting the infection. Hutchinson be- 
lieves that infection is spread largely by uncooked fish, in confirma- 
tion of which opinion he points to the prevalence of the disease in 
fish-eating communities. How infection is acquired is not definitely 
known: should we believe Hutchinson, it may be acquired by inges- 
tion; it may be acquired by inhalation — witness the lesions in the 
nose, believed by some observers to be an initial lesion; and the 
frequency of leprosy of the hands and the feet (often uncovered), to- 
gether with the presence of lepra bacilli in the earth, suggests that infec- 
tion may be acquired by direct inoculation through wounds. Heredity 
is of little, if any, etiological influence; the youngest subjects are rarely 
less than three to six years of age; beyond this no age is exempt. 

Pathology. — Leprosy is one of the so-called granulomas. The 
lesions consist of nodular masses or diffuse infiltrations made up of 
small rounded and fusiform cells, larger endothelial often vacuolated 
cells, and giant cells, in and between which the lepra bacilli are found 
in profusion. These lesions are found usually in the skin, the mucous 
membranes, and the viscera. On the surface the lesions not infre- 
quently progress to softening and ulceration attended by marked loss 



LEPROSY 167 

of tissue and noteworthy mutilation. In the nerves nodular and diffuse 
infiltrations are observed, with overgrowth of the connective tissue and 
atrophy of the axons. Changes analogous to tabetic arthropathy are 
sometimes observed in the bones. The lymph nodes are often palpably 
enlarged. 

Symptoms. — The period of incubation is from three to five years 
(Hansen), but a case of presumed direct inoculation has been observed 
in which the period of incubation was four weeks. Some observers 
believe in the existence of a primary sore (the existence of which is not 
altogether unlikely), and have located it commonly in the nose (where 
they have observed ulceration), but the evidence is not yet conclusive. 
During the period of incubation the patient suffers from irregular attacks 
of fever, malaise, headache, and pains in the joints. In many cases 
the initial manifestations consist of dusky red erythematous and hyper- 
esthetic patches on the skin, especially of the face, extensor surfaces 
of the hands and forearms (macular leprosy); these soon become pig- 
mented, later anesthetic, and gradually lose their pigment and become 
white (lepra alba). Soon the disease takes on the characters of one of 
the two well-recognized types, the nodular (tubercular) or anesthetic; 
but commonly the disease is of mixed type. 

The nodular type is characterized by the development of nodules, 
varying in size from that of a pea to that of a cherry, and of diffuse 
fibrous infiltration of the skin and the mucous membranes. Beginning 
usually in the skin of the face (nose, lips, or chin) or the ears, they 
produce painless, irregular thickenings, nodosities, and folds, leading 
to much distortion and ultimately to the condition known as facies 
leontina. Gradually nodules and thickenings develop elsewhere, 
especially on the hands, forearms, feet, legs, buttocks, knees, etc., until 
much of the cutaneous surface is involved. Occasionally some of the 
nodules lessen in size, and even disappear, but usually they soften and 
ulcerate, and thus add to the already existing deformity. Involvement 
of the mucous membrane of the nose, mouth, throat, and larynx is 
evident in the nasal discharge, hoarseness, aphonia, dyspnoea, etc., 
and is quite manifest upon local examination — irregular nodular and 
diffuse thickenings and ulcerations. Inhalation pneumonia not infre- 
quently results; and from involvement of the conjunctiva and cornea 
blindness may ensue. The disease runs a course of years (five to ten 
or more), and ultimately leads to death from exhaustion or from pul- 
monary or other complications. 

The anesthetic type manifests itself, in addition to the macules already 
mentioned, by early pain in the limbs and areas of hyperesthesia and 
paresthesia, followed by anesthesia (often only analgesia) and trophic 
lesions (bullae) of the skin of the extremities. Anesthetic areas, how- 
ever, may develop without preceding macules, and not infrequently 
become extensive. The bullae often break down and lead to the forma- 
tion of extensive perforating ulcers and widespread destruction of tissues. 
The nerve trunks are often palpably thickened; the muscles waste; 



168 NON-BACTERIAL FUNGUS INFECTIONS 

the fingers become clubbed and contracted (claw-like) ; wasting, necrosis, 
and gangrene ensue; and the fingers and toes may drop off (leprosy 
mutilans); or arthropathies (resembling those of tabes) may develop. 
The lesions pursue an extremely chronic course (ten to thirty years), 
and ultimately lead to death through exhaustion or an intercurrent 
infection. 

Diagnosis. — In advanced cases the diagnosis is unmistakable. In 
the early stages the dusky red areas of erythema, at first hyperesthetic, 
later anesthetic, and devoid of pigment; the nodular neuritis; and the 
detection of lepra bacilli in the nasal secretion or in an excised nodule, 
suffice for diagnosis. Serum diagnosis — the agglutination of the lepra 
bacilli by the blood serum of a leprous patient — may prove of some 
service. 

Prognosis. — The patients frequently live from ten to thirty years, 
unless carried off by an intercurrent infection. In some cases the 
disease seems to have been entirely arrested. 

Treatment. — Segregation is advisable in all cases. Special attention 
should be paid to general hygienic measures, and the patient should 
have an abundance of good nutritious food, of sunshine, and of fresh 
air. Recently almost specific properties have been claimed for chaul- 
moogra oil, 10 minims, gradually increased to 2 drams, three times daily. 
Dyer reports several cures from its use. Dyer has also had good results 
from Calmette's antivenene. Gurjun oil, ichthyol (Unna), mercuric 
bichloride, salicylic acid, and many other remedies have been recom- 
mended from time to time. A supposed antileprous serum also has 
been introduced of late. Nastine, a bacterial fat recommended by 
Deycke, does not seem to be of much value. 



NON-BACTERIAL FUNGUS INFECTIONS. 

The non-bacterial fungus infections comprise a group of diseases 
caused by microorganisms that are sometimes described as higher bac- 
teria, sometimes as fungi, but which probably represent low forms of 
life intermediate between the bacteria and the more highly developed 
fungi. They have been incompletely studied and classified, but Park 
suggests the following attempt at differentiation: (1) Actinomyces, 
characterized by radiating wreath-like forms which it alone produces 
in the living body. (2) Streptothrix, characterized by an abundant 
true branching, wavy growth, later fragmentation, and the formation 
of conidise, which serve as organs of propagation, and in this sense may 
be considered as spores. (3) Cladothrix, characterized by false branch- 
ing, rapid fragmentation, and then bacillary characteristics in old cul- 
tures. (4) Leptothrix, characterized by lack of observed branching, 
non-wavy growth, but, on the contrary, stiff, almost straight threads, in 
which division processes are seldom or never observed. 



ACTINOMYCOSIS 169 



ACTINOMYCOSIS. 



Actinomycosis is a chronic, specific, infectious disease caused by Strep- 
tothrix actinomyces, or ray fungus, and characterized by the develop- 
ment of a chronic granuloma that ultimately softens and discharges 
characteristic actinomycotic granules.- 

Etiology. — Actinomycosis is common in cattle, in whom it causes 
"big jaw" and "wooden tongue," in horses, and in pigs. It is believed 
to be non-contagious, since direct transference from the sick to the well 
is not observed. Inasmuch as the fungus occurs on grain, such as 
oats, barley, rye, etc., infection is probably acquired with the food — 
certainly in the lower animals. In man infection may be acquired in a 
similar manner, an abrasion of the mucous membrane or a carious 
tooth (in which the fungus has been found) being probably the infectious 
atrium; but it may be acquired also by inhalation (as at threshing, for 
instance), or through a cutaneous wound. The disease is three times 
as common in men as in women. 

Pathology. — Actinomycosis is one of the so-called infectious granulomas, 
and consists of foci of epithelioid cells, giant cells, small round cells, and 
the fungus, and the later development of marked hyperplasia of the con- 
nective tissue — a condition not altogether unlike tuberculosis; but so 
great is the enlargement that it is sometimes mistaken for sarcoma. 
Later softening and suppuration occur and many sinuses form, from 
which issues a thin, sanious, purulent fluid containing characteristic, 
small, sulphur-yellow, actinomycotic granules which, upon microscopic 
examination, reveal the ray fungus. 

Symptoms. — Almost any organ of the body may be involved, but for 
obvious reasons, the jaw and the adjacent tissues are most frequently 
affected. Usually a firm, indurated mass develops; this gradually 
increasing in size, ultimately softens, whereupon its contents are dis- 
charged through several sinuses. In consequence of involvement of the 
periosteum and the bone, necrosis not infrequently ensues, and gradu- 
ally other organs become implicated, such as the tongue, the tissues of 
the neck, the ear, and sometimes even the meninges, from direct exten- 
sion, and more distant organs, such as the liver, the lung, the brain 
(symptoms of tumor), by metastasis. The region of the cecum and 
appendix is not infrequently the seat of primary involvement, but any 
part of the large or the small intestine may be involved, and the actino- 
myces may be found in the stools.- The liver is rather frequently the 
seat of secondary abscesses (reticulated or honey-combed abscesses). 
The lungs may reveal miliary actinomycosis, fetid bronchitis, chronic 
interstitial pneumonia, or bronchopneumonia, which may progress to 
abscess or cavity formation or gangrene; the actinomyces may be found 
in the sputum. The pleura may be markedly thickened, and from 
this by contiguity the adjacent soft parts, the ribs, or the vertebrae may 



170 NON-BACTERIAL FUNGUS INFECTIONS 

become involved. Cutaneous lesions and chronic suppurative and ulcer- 
ative processes have occasionally been observed. 

Diagnosis. — The disease may be suspected in cases of long-standing 
suppuration with a tendency to involvement of the bones, but it is con- 
firmed only by finding the specific cause, the actinomyces. 

Prognosis. — The prognosis depends largely upon the extent of the 
lesions and whether or not they are amenable to surgical intervention. 

Treatment. — The treatment is primarily surgical. But recently in view 
of the success that has attended its administration potassium iodide, 
upward of one dram (4 grams) daily, has come to be looked upon as 
almost a specific. Good results have also attended the use of the 
ir-rays. 

MYCETOMA. 

(Madura Foot.) 

Mycetoma is a chronic, specific, infectious disease caused by Strep- 
tothrix madurse or Streptothrix mycetomas, and characterized by nodular 
enlargement and deformity proceeding to oily degeneration and sinus 
formation. 

Etiology. — Mycetoma has been observed, usually sporadically, in 
Asia, Europe, South America, and the United States. It is most common 
between the twentieth and the forty-fifth year, and occurs more frequently 
in men (especially those who go bare-footed) than in women. How 
infection occurs is not definitely known, though it is not unlikely through 
a wound or abrasion, or, as some believe, through the sweat glands. 

Symptoms. — Two varieties of mycetoma are recognized, the melanoid, 
or mycetoma with black granules, and the ochroid, or mycetoma with 
yellowish or white granules — due respectively to Streptothrix madurse 
and Streptothrix mycetomas. The disease begins with the development 
of a hard, firm, painless nodule on the sole of one foot, usually the right, 
though other parts may be affected, such as a toe, the hand, or a finger. 
The nodule soon softens and at the end of about a month ruptures and 
discharges a peculiar, viscid, oily, slightly purulent, and sometimes blood- 
streaked fluid in which the blackish or yellowish granules are suspended. 
Similar lesions develop elsewhere in the foot, which ultimately becomes 
much enlarged. The lesions gradually attack the muscles, ligaments, 
and bones and convert them into a thick, greasy, yellowish mass into 
which a probe may be inserted in any direction to a considerable depth 
without provoking pain or hemorrhage. The lesions show little or no 
tendency to heal, the sinuses being, as a rule, permanent. As the foot 
enlarges and can no longer be used, the leg atrophies from disuse. In 
some cases the lesions tend to spread along the lymphatics and set up 
new foci of infection. The general health remains unimpaired for a 
long time; the patient may live ten or twenty years, but ultimately 
succumbs to exhaustion or an intercurrent infection. 

Diagnosis. — The disease is only likely to be mistaken for actinomy- 
cosis to which the disease is much allied. Doubtless many of the cases 



1 



PULMONARY ASPERGILLOSIS 171 

reported, especally in this country, were really actinomycotic. The 
differential diagnosis is to be made largely by a microscopic examination 
of the discharge. In some cases the lesions may simulate those of 
syphilis or sarcoma. 

Treatment. — The treatment consists of resection if a small area only 
is involved, and of amputation if the disease is more widespread. The 
amputation must be done well above the infected area. Potassium 
iodide is useless. 

NOCARDIOSIS. 

(Streptothricosis ; Cladothricosis; Pseudotuberculosis; Atypical Actinomycosis.) 

Nocardiosis is a generic term, suggested by Wright, to describe a group 
of diseases caused by nocardia, microorganisms to which the terms 
streptothrix, cladothrix, pseudotubercle bacillus, and atypical actin- 
omycosis have also been applied. 

Etiology. — These nocardia are widely distributed in nature. Infection 
is usually acquired through inhalation, rarely by means of cutaneous or 
mucous membrane wounds; and it is predisposed to by general malnutri- 
tion. The infection is rare in man. 

Pathology. — The lesions consist of inflammation, necrosis, suppuration, 
abscess formation, and granulation tissue. In some cases the lesions 
resemble tuberculosis, that is, there are tubercles, flbrocaseous nodules, 
and calcification. The lesions are most common in the lungs; metastases 
have been observed in the brain, kidney, myocardium, lymph nodes, etc. 

Symptoms. — The process may be acute or chronic. The symptoms 
vary, depending upon the seat of the lesions, but in general they are those 
of inflammation and suppuration. When occurring, as is common, in 
the lung, the symptoms are those of pneumonia, abscess, tuberculosis, or 
empyema. In the brain, the symptoms are those of abscess, tumor, or 
meningitis. Multiple abscesses may occur in the skin and subcutaneous 
tissues. 

Diagnosis. — Occasionally the symptoms have been somewhat atypical 
of the disease suspected, but, as a rule, the diagnosis depends solely upon 
detecting the causative microorganism in the sputum or other discharge 
or fluid of the body. 

Prognosis. — The outlook is bad, since the great majority of the sub- 
jects finally succumb. 

Treatment. — There is no specific treatment. In general, the treatment 
is that of the disease suspected — pneumonia, tuberculosis, abscess of the 
lung, etc. Abscesses should be treated surgically. 



PULMONARY ASPERGILLOSIS. 

Pulmonary aspergillosis is a chronic disease caused by Aspergillus 
fumigatus and characterized by inflammation and necrosis of the lung. 



172 NON-BACTERIAL FUNGUS INFECTIONS 

Etiology. — Aspergillus fumigatus is widely distributed in nature, and 
is often found as a harmless parasite on different surfaces and in certain 
cavities of the body. Most of the cases of infection occurring in man are 
secondary or terminal, developing especially in tuberculosis; but appar- 
ently primary cases have been observed. The infection is believed to 
be acquired from infected birds or infected seed fed to birds (occurring 
thus in pigeon feeders), or from the dust of rye flour used to remove 
grease from hair (whence the infection occurs in hair-sorters). 

Pathology. — The lesions consist of inflammatory processes akin to those 
of bronchopneumonia, in the midst of which the fungus may be en- 
countered. From coalescence of adjacent foci more or less widespread 
solidification may occur. Ultimately necrosis and softening may ensue, 
cavity formation develop, and gangrene may supervene. 

Symptoms. — The symptoms are those of chronic tuberculosis, chronic 
interstitial pneumonia, bronchiectasis, etc., and aside from the presence 
of the fungus in the expectoration may not present special characteristics. 

Diagnosis. — The diagnosis depends upon detecting the fungus in the 
sputum. In most cases, cases of secondary or terminal infection, the 
infection may be of minor importance; the tubercle bacillus may be 
found associated with the fungus. 

Prognosis. — The outlook is bad, largely because of the associated 
conditions. 

Treatment. — The treatment is that of the underlying disease, such as 
tuberculosis, etc. Arsenic and potassium iodide have also been recom- 
mended. Prophylactic measures, looking to the avoiding of inhaling 
infected, dust-laden atmosphere, should be undertaken with a view to 
prevent the primary cases. 



OIDIOMYCOSIS. 

(Blastomycosis; Saccharomycosis; Blastomycetic Dermatitis; Protozoic Dermatitis; 
Dermatitis Coccidioides; Coccidioidal Granuloma; Psorospermiasis.) 

Oidiomycosis is a chronic infectious disease of the skin and internal 
organs caused by fungi of the genus Oidium, and characterized by granu- 
lomatous inflammation proceeding to suppuration. 

Etiology. — The organism is widely distributed in nature, but the factors 
leading to infection in man are not well understood. 

Pathology. — The lesions may be limited to the skin or the lungs, or 
they may involve also other organs, such as the liver, spleen, kidneys, 
adrenals, lymph nodes, meninges, etc. In general they consist of granu- 
lomatous formations tending to softening and abscess formation. In 
some cases the slow progression of the lesions and the absence of soften- 
ing suggest tuberculosis. In the skin the lesions may simulate those of 
tuberculosis or squamous epithelioma. 

Symptoms. — In the skin the symptoms consist of the development of a 
papular or pustular area, which gradually increases in size to form a 






PROTOZOAN INFECTIONS 173 

rough, scaly, elevated fungus-like surface, variously the seat of minute 
abscesses and of scars in different stages of cicatrization. In the lungs 
and other viscera the symptoms are analogous to those of tuberculosis. 

Diagnosis. — The diagnosis depends upon the detection of the causative 
microorganism. 

Prognosis. — The disease is chronic, lasting many years. When limited 
to the skin the process may be brought to a standstill or cured ; but when 
the viscera become involved death usually eventually ensues. 

Treatment. — Potassium iodide in large doses (150 grains, 10 grams, 
daily) has been followed by good results in some cases. The arrays are 
also of service in some cutaneous lesions; or these lesions may be curetted, 
excised, or treated with antiseptics. 



ZOOPARASITE INFECTIONS. 



PROTOZOAN INFECTIONS. 

The protozoa are unicellular animal organisms that reproduce by 
division or sporulation. There are four important phyla (tribes) or 
primary divisions : 

1. Sarcodina, protozoa that throw out changeable protoplasmic 
processes, called pseudopodia, which serve the double purpose of nutri- 
tion and locomotion. To these belong the class Rhizopoda (those with 
lobose or reticulose pseudopodia). These include: Entamoeba dysenteric 
(or histolytica), the cause of one form of dysentery; Entamoeba coli, 
believed to be a harmless intestinal parasite; and Leydenia gemmipara, 
which has been found in ascitic fluid in cases of carcinomatosis, but is 
perhaps of no pathogenic significance. 

2. Mastigophora, protozoa provided with undulating membranes 
or flagella that serve as means of locomotion and obtaining food. To 
these belong the class Flagellata (small forms with one or several flagella). 
These include: (a) Spirochete (spiral in shape and provided with an 
undulating membrane, but no flagella), of which Spirochseta recurrentis 
(or obermeieri) is the cause of relapsing fever of Europe, and is perhaps 
related to Spirochaeta carteri (relapsing fever of India), Spirochseta novyi 
(relapsing fever of America), and Spirochseta duttoni (relapsing fever 
of Africa); Spirochseta vincenti is found, associated with a fusiform 
bacillus, in some cases of inflammation of the throat, called Vincent's 
angina; and Spirochseta refringens is found in ulcerations of the genitalia, 
and is often associated with Treponema pallidum in syphilitic lesions. 
(b) Treponema?, those with a flagellum at both ends, but without an 
undulating membrane. Of these, Treponema pallidum is the cause of 
syphilis; and Treponema pertenuis is believed to be the cause of yaws 



174 PROTOZOAN INFECTIONS 

(framboesia). (c) Trypanosomas, those with a more or less spiral-shaped 
body, along one side of which there is an undulating membrane from 
which a flagellum projects. Of these, Trypanosoma gambiense is the 
cause of human trypanosomiasis, or sleeping sickness. The following 
trypanosomes also are found in mammals: Trypanosoma lewisi, which 
infects rats, but seems usually not to occasion noteworthy symptoms; 
Trypanosoma evansi, the cause of surra in horses and mules, especially 
in India and the Philippines; Trypanosoma brucei, the cause of nagana 
in horses, and found also in many game animals in Africa ; Trypanosoma 
equiperdum, transmitted by coitus, the cause of dourine (maladie du 
coit) in horses and donkeys; Trypanosoma equinum, the cause of 
mat de caderas in horses in South America; Trypanosoma theileri, the 
cause of galziekte (gall sickness) in cattle ; and Trypanosoma dimorphon, 
the cause of Gambian horse disease, (d) Leishmania (oval intracellular 
parasites), of which Leishmania donovani is the cause of kala-azar, and 
Leishmania tropica is the cause of oriental sore, (e) Trichomonas, 
a parasite with a fusiform body, an undulating membrane and three 
flagella arising from its anterior end. These include: Trichomonas 
vaginalis, which is common in acid vaginal mucus; and Trichomonas 
(or Cercomonas) hominis, which is found in the intestine, where appar- 
ently it may set up an acute enteritis ; and it may invade or be introduced 
into the bladder and set up cystitis. (/) Lamblia intestinalis (a pear- 
shaped, flagellated organism), which is common in the intestine, where 
it may perhaps set up acute or chronic diarrhoea; it has been found also 
in the expectoration of bronchiectasis and gangrene of the lung, in pleural 
exudates, etc. 

3. Infusoria, protozoa with cilia. To these belong the ciliata (those 
with contractile vacuoles and many fine cilia which are shorter than 
flagella and exhibit a sweeping motion). These include Balantidium coli, 
a parasite that is common in hogs, and may set up a dysenteric disorder 
in man. 

4. Sporozoa, protozoa without motile organs, that reproduce by 
sporulation. These include: (a) Coccidiaria, of which Eimeria stiedse 
(Coccidium cuniculi or oviforme) is most frequently found in the epithe- 
lium of the bile ducts of animals, especially rabbits, and the oocyst of 
which may be found in the feces. The disorder is known as coccidiosis; 
several cases have been reported in man. Isospora bigemina (Coccidium 
bigeminum) is common in the intestine of dogs and cats, and has been 
observed in the human subject, (b) Hcemosporidia, of which Plasmodium 
malarias is the cause of malarial fever. Similar organisms have been 
found in other animals: Plasmodium kochi in monkeys; Plasmodium 
prsecox in birds (causing proteosoma; halteridium in crows and pigeons); 
and other hsemosporidia in other animals. 



A MCE BIAS IS 175 

AMEBIASIS. 

(Amoebic Dysentery; Amoebic Colitis.) 

The common manifestation of amoebiasis is an acute or chronic in- 
flammation and ulceration of the colon caused by Entamoeba dysenteriae 
(or histolytica). Schaudinn, Craig, and others distinguish two forms 
of amoebae that may be found in the intestine, the pathogenic Entamoeba 
dysenteriae, and Entamoeba coli, believed to be a harmless, non-patho- 
o-enic form. 

Etiology. — Amoebic dysentery is endemic in the tropics, where it is a 
very common, if not the commonest form of dysentery encountered. 
Sporadic cases occur from time to time throughout the subtropical and 
the temperate zones, and epidemics are by no means unknown. The 
disease is most common in young male adults; it prevails especially 
among the poor, and it is predisposed to by general malnutrition and 
unhygienic surroundings. The infection is usually transmitted by the 
drinking water. 

Pathology. — The lesions may involve the entire colon, and sometimes 
even the lower part of the ileum ; but they are most common and, as a rule, 
most marked in the cecum, in the hepatic and sigmoid flexures, and in the 
rectum. They consist of inflammation, oedema, and cellular infiltra- 
tion of the submucosa, which are soon followed by necrosis and ulcera- 
tion. In the early stages there are localized areas of thickening and 
infiltration, the mucous covering of which soon becomes soft and necrotic, 
and eventually being discharged, leaves a roundish, ovoid, or irregular 
ulcer. The base of the ulcer is often much larger than the point of dis- 
charge of the necrotic tissue, that is, the edges of the ulcer are undermined 
or overhanging; and adjacent ulcers often communicate by means of 
sinuous tracts, the mucosa overlying which may be more or less normal, 
although it is usually more or less thickened and inflamed. The floor 
of the ulcer may be made up of the submucosa, the muscularis, or the 
serosa; or it may be adhesions that bind the colon to adjacent organs 
or tissues. Perforation may occur into these adhesions or into the 
surrounding connective tissue or the peritoneum. In advanced cases, 
the intestinal wall is much thickened and infiltrated, and the seat of 
numerous and extensive ulcerations, with here and there areas of more 
or less intact mucosa; or there may be widespread sloughing, pseudo- 
membrane formation, or gangrene. Healing of the ulcerations and 
cicatrization occur irregularly and to a varying degree, and they lead to 
more or less deformity and partial obstruction (stricture) of the bowel. 
Microscopic examination reveals the ordinary changes of inflammation 
and ulceration, with, however, only moderate polynuclear leukocytic 
infiltration: necrosis rather than suppuration being conspicuous. In 
chronic cases there is also considerable connective tissue proliferation. 
The amoebae may be found in the base of the ulcer, in the adjacent 
lymph spaces, and sometimes in the bloodvessels — whence they are 



176 PROTOZOAN INFECTIONS 

readily conveyed to the liver, where they give rise to widespread necrosis 
and a so-called amoebic abscess. The amoebae may be cultivated, with 
difficulty, from the intestinal discharges, the intestinal wall, and the liver 
abscesses. In the intestinal tract they may be associated with other 
protozoa, such as trichomonas, cercomonas, etc., and with various 
metazoa, such as Taenia saginata, Ascaris lumbricoides, Uncinaria 
duodenalis, etc. They have been found also in the peritoneal cavity, 
the pleura, lung, bladder and urine, abscess of the mouth, necrosis of 
the jaw, etc. 

Symptoms. — Strong divides the cases into three classes, which, how- 
ever, are not sharply demarcated the one from the other: (1) Mild cases 
and those of moderate severity; (2) cases with acute onset; and (3) 
advanced and chronic cases. In the mild cases the onset is insidious, 
the patient often being unable to state when the disease began. The 
chief symptoms consist of more or less abdominal pain and diarrhoea; 
the diarrhoea may be periodic and may alternate with constipation. 
The stools may contain mucus and the amoebae; often little if any blood. 
In addition there may be such general symptoms as lassitude, headache, 
loss of weight, etc. The disorder may last for months, the mildness 
of the symptoms often warranting the terms latent or masked infection; 
but the disorder may become aggravated and pass on to one of the other 
types. The cases with acute onset may represent an acute infection or 
an acute exacerbation of a mild or latent infection. The chief symp- 
toms consist of abdominal pain (tormina), frequent stools containing 
mucus, blood, and the amoebae, and more or less constant and distressing 
tenesmus. Sloughs of the bowel also may be passed. Usually there is 
abdominal tenderness, especially along the course of the colon, moderate 
fever, and the patient emaciates rapidly. The pulse may become rapid 
and feeble, and death may ensue within a week or ten days from asthenia, 
toxemia, syncope, hemorrhage, or peritonitis from perforation. In 
other cases, after four or five days, the acute manifestations subside and 
may eventually disappear, or the condition may become chronic. The 
advanced and chronic cases may result from the acute cases or they 
may be subacute or chronic from the beginning. They are characterized 
by alternating periods of diarrhoea and constipation; the diarrhceic 
attacks are characterized by abdominal pain, frequent stools containing 
mucus, blood, and the amoebae, more or less tenesmus, and slight or 
moderate fever. There may be more or less emaciation and impair- 
ment of the general health; so-called indigestion, and provoking of the 
attacks apparently by dietetic indiscretions. The tongue is likely to be 
red and raw-looking. The condition may last for six months, or a year 
or more. In the protracted cases emaciation may be extreme, and death 
may eventually ensue. 

Complications and Sequels. — Liver abscess is common; it may involve 
the lung and lead to a so-called hematopulmonary abscess. Intestinal 
perforation and peritonitis, arthritis, etc., also occur, 



AMEBIASIS 177 

Diagnosis. — The diagnosis is readily made from attention to the bloody 
mucous character of the stools, and the detection therein of the amcebse. 
The liver should always be carefully studied for signs of abscess (en- 
largement, local pain or discomfort, chills, fever, sweats, and leukocytosis). 

Prognosis. — The mild cases usually yield to treatment, but relapses 
are common. In chronic cases the outlook is not encouraging, but with 
care and attention recovery may be brought about. 

Treatment. — The prophylactic measures mentioned on page 29 should 
be carried out, since there is much reason to believe that the disease is 
spread and acquired as is typhoid fever. During the acute stage the 
patient should be in bed. The diet should be the blandest — milk 
(peptonized or diluted with barley water, lime water, or Vichy water), 
albumin water, raw eggs, beef juice, broths, custard, milk toast, etc. 
In subsiding or chronic infections the greatest attention also must be 
paid to the diet, since recurrences are not infrequently provoked by 
dietetic indiscretions. At the beginning of an attack, especially if there 
has been little diarrhoea, the bowels should be cleared with blue mass, 
calomel, or castor oil to which 20 minims (1.25 c.c.) of tincture of opium 
may be added. Ipecac is believed by men of large experience to exert 
an almost specific effect, and assuredly should be tried. Not less than 
three hours after the patient has had food, mild counterirritation (a 
mustard plaster or tincture of iodine) should be applied to the abdomen, 
and 10 to 15 minims (0.6 to 1 c.c.) of tincture of opium given by the 
mouth, or \ grain (0.015 gram) of morphine administered hypodermicly. 
After the lapse of ten to fifteen minutes, 30 to 60 grains (2 to 4 grams) 
of freshly powdered ipecac root should be administered, preferably in 
salol-coated pills or capsules. The patient must maintain the recumbent 
posture for several hours : this as well as the salol-coated pills or capsules 
tend to obviate nausea and vomiting; but should vomiting occur, the dose 
of ipecac should be repeated after a short interval. Decreasing doses 
(5 to 10 grains, 0.3 to 0.6 gram, less than the initial dose) should be given 
on succeeding days. The use of purgative doses of sodium or magnesium 
sulphate has also been much commended: one dram (4 grams) at fre- 
quent intervals (every fifteen to thirty minutes) until the intestine has 
been thoroughly cleansed, whereupon aromatic sulphuric acid (believed 
to be detrimental to the infecting microorganisms) may be given in rather 
large doses. Irrigation of the bowel is of great advantage in many cases, 
but the pain and tenesmus are often obstacles to its use in acute cases; 
but sometimes these may be lessened by a preliminary enema of tincture 
of opium (J to 1 dram, 2 to 4 c.c.) and thin starch water (2 to 4 ounces, 
60 to 120 c.c). The irrigation should be done by means of a fountain 
syringe, and the tube should be inserted high up; the best solution is 
quinine, 1 to 5000 gradually increased to 1 to 1000, of which one to two 
quarts should be injected twice daily and retained, if possible, for at least 
fifteen minutes. Ice-water enemas also may prove grateful. The rectal 
tenesmus may be relieved by an opium and belladonna suppository. 
12 



178 PROTOZOAN INFECTIONS 

In chronic cases that do not improve on medical treatment, resort may 
be had to colostomy or appendicostomy and drainage and irrigation of 
the colon through the wound. 



RELAPSING FEVER, 

{Recurring Fever; Seven Day Fever; Famine Fever; African Tick Fever; 
Spirochetosis; Spirillosis.) 

Relapsing fever, originally believed to be a single, acute, specific, 
infectious disease characterized by alternating periods of fever and of 
apyrexia of about six days each, is now known to include at least four 
forms of such fever, each more or less distinctive, more or less limited 
in geographical distribution, and caused by four species of spirochetes: 
Spirochaeta recurrentis (Spirillum obermeieri), the cause of the relapsing 
fever of Europe, especially of Russia, the Balkans, etc.; Spirochaeta 
duttoni, the cause of the relapsing fever of Africa (African tick fever); 
Spirochaeta carteri, the cause of the relapsing fever of India; and Spiro- 
chaeta novyi, the cause of the relapsing fever of America. 

Etiology. — The disease prevails especially amidst destitution, squalor, 
and general unhygienic surroundings. Personal factors, such as age, 
sex, and race, as well as climate and season, are without special etiologi- 
cal significance, although the disease is said to prevail especially among 
young adults, and during the winter. One attack confers a partial 
immunity. 

The exciting cause of the disease is one of the aforementioned spiro- 
chetes. The infection is believed to be transmitted by insects or ticks. 
This has been definitely proved in the case of Spirochaeta duttoni, a 
tick, Ornithodorus moubata, being the transmitting agent. The bed-bug 
(Cimex lectularius) is believed to be the transmitting agent of Spirochaeta 
recurrentis, and the body-louse (Pediculus corporis) that of Spirochaeta 
carteri, but the evidence is not yet conclusive. Nothing is known of the 
mode of transmission of Spirochaeta novyi. Nor has it yet been definitely 
determined whether the transmission is purely mechanical or whether 
the spirochetes undergo some developmental process within the body 
of the transmitting insects or ticks. 

Pathology. — There are no characteristic lesions. The spleen is en- 
larged and soft; the liver, kidneys, heart, etc., reveal parenchymatous 
degeneration and, occasionally, hemorrhagic infarction; and the bone 
marrow has been found hyperplastic. 

Symptoms. — The period of incubation is from five to eight days. 
Usually without prodromal symptoms, the disease begins suddenly, 
with severe chill, high fever, rapid pulse (120 to 140 per minute), general 
neuromuscular pains and sensitiveness, extreme prostration, and some- 
times delirium. In children and adolescents there may be nausea and 
vomiting, rarely convulsions. By the end of twenty-four or thirty-six 
hours, the temperature has attained its maximum (105° to 106° F.), 



RELAPSING FEVER 179 

and it continues high with slight morning remissions. During the period 
of fever, the spleen is much enlarged and palpable, and there may be 
jaundice, nausea, vomiting, slight bronchitis, profuse sweating, sudamina, 
herpes labialis, slight albuminuria, stupor, delirium, and a slight leuko- 
cytosis. After the lapse, usually of six (sometimes five, or seven, rarely 
ten) days, the temperature falls rapidly within twelve hours or less, to the 
normal or below, the patient sweats profusely, or has a critical diarrhoea, 
and by the following day feels almost entirely well, although there may 
be a slight elevation of temperature for a day or two. Rarely there is but 
a single paroxysm, but in most cases, on or about the fourteenth day, that 
is, after a period of apyrexia, lasting six or seven days, a severe chill 
occurs, and the febrile attack is repeated; sometimes there is a third, 
fourth, and even fifth relapse. Usually the succeeding paroxysms are 
of decreasing severity and duration. In unusual (toxic) cases, a typhoid 
condition with marked delirium and coma, sometimes petechial hemor- 
rhages, localized necrosis of the mucous membranes, and bed sores, 
develop, and death occurs from toxemia and cardiac collapse. 

The African tick fever resembles the other types of relapsing fever, but 
it may differ in some respects : the periods of fever may be as short as 
three days, the periods of apyrexia may be irregular (one day to three 
weeks), diarrhoea and dysentery may be present, etc. 

Complications. — Complications are rare. The most common are pneu- 
monia, sepsis, ititis, choroiditis, neuritis (with consequent paralysis), 
rupture of the spleen, gastro-intestinal catarrh, and hemorrhage from the 
kidneys, nose, gastro-intestinal tract, etc. 

Diagnosis. — In the early stages the disease may be mistaken for typhoid 
or typhus, and even yellow fever, but the subsequent course of the disease 
and the results of examining the blood are conclusive. The spiro- 
chetes may be found in the peripheral blood during the period of fever; 
they lessen in number with the decline of the fever, and they are absent 
after the crisis and during the periods of apyrexia, although the blood 
remains infectious to susceptible animals. The recurrence of the parox- 
ysms at regular intervals indicates the protozoan nature of the parasite 
and that it passes through a definite cycle of development. A form of 
lymphatic tuberculosis, clinically resembling pseudoleukemia, or Hodg- 
kins' disease, much simulates relapsing fever, but the paroxysms of fever 
and of apyrexia are more irregular in course, development, and frequency; 
the lymph nodes may be enlarged, the spirochete is absent from the blood, 
and the patient may react to tuberculin injections. Irregular forms of 
malaria may be distinguished by the course of the fever and the results 
of examining the blood. 

Prognosis. — The prognosis is good in the absence of extreme severity 
of infections and complications. The mortality rate is low — 2 to 4 
per cent. 

Treatment. — Efforts should be made to prevent the infection by in- 
culcating and practising habits of personal and domestic cleanliness, 
by avoiding vermin-infested places, and the use of beds high from the 



180 PROTOZOAN INFECTIONS 

ground and protected by mosquito netting, or of hammocks suspended 
by ropes. The treatment of the developed disease,which must be based 
upon general principles, consists largely of good hygienic surroundings, 
good nursing, and good food. The symptoms are to be treated symp- 
tomatically — the high fever by cold sponging, the neuromuscular pains 
by local applications, embrocations, and anodynes, such as Dover's 
powder internally or morphine subcutaneously. Toxemia and cardiac 
debility are to be treated on general principles. The evidence in favor 
of an antispirochetic serum is not yet conclusive; Novy and Knapp have 
had success in curing the infection in rats with an immune serum. 



SYPHILIS. 

{hues; The Pox.) 

Syphilis is a chronic, specific, infectious, congenital or acquired 
disease, caused by Treponema pallidum (Schaudinn and Hoffmann); 
it is characterized, when acquired, by a so-called primary lesion, the 
chancre, at the seat of inoculation; certain constitutional disturbances, 
and disorders of the skin, mucous membranes, and lymph nodes (so-called 
secondaries); specific granulomatous growths in the viscera, blood- 
vessels, bones, muscles, skin, and mucous membranes (so-called ter- 
tiaries); and sometimes by certain so-called parasyphilitic or meta- 
syphilitic diseases of the nervous system, especially tabes dorsalis and 
general paresis (so-called quartanaries). Aside from the primary lesion, 
the lesions of the congenital form of the infection do not differ essentially 
from those of the acquired form. 

Etiology. — Syphilis prevails in all parts of the world; it is peculiarly 
a disease of mankind, and occurs at all ages and in both sexes. Until 
recently the lower animals were believed to be immune, but Metch- 
nikoff and Roux have shown that experimentally the infection can be 
transmitted to the anthropoid apes. The specific infectious agent is 
Treponema pallidum, which may be demonstrated in the blood and in 
the lesions. 

Acquired syphilis is usually, but not always, transmitted by sexual 
intercourse, or perversions thereof. But the disorder is not always a 
lues venera, since it may be transmitted by way of the lips in kissing, 
and by way of even slight abrasions or wounds of the skin or mucous 
membranes, such as of the fingers and hands of physicians, surgeons, 
obstetricians, and nurses, of the breast of wet nurses (syphilitic child), 
etc.; and it may also be transmitted indirectly by means of divers 
fomites, such as infected drinking and eating utensils, pipes, dental 
instruments, clothing, tattooing instruments, etc., and formerly by 
vaccine virus when human lymph was employed. The blood and the 
secretions from the primary, secondary, and tertiary lesions containing 
the specific infectious agent may transmit the disease if they come in 
contact with an abraded skin or mucous membrane. The normal 



SYPHILIS 181 

physiological secretions, such as the milk, tears, sweat, and urine, are 
ordinarily non-infectious, but they readily become infectious through 
contamination with the secretions of a syphilitic sore; the saliva and 
the semen are usually infected (through contamination). 

Congenital syphilis may be transmitted in one of several ways: (1) 
By the father (sperm transmission), the mother being healthy. This 
is very common, the semen carrying the infectious agent, and infecting 
as it fertilizes the ovum. It is more likely to occur the more recent the 
infection in the father; it is unlikely after the lapse of three or four 
years, if the man has been efficiently treated; but it may occur even 
after years of apparently complete recovery and entire absence of 
symptoms. On the other hand, a man with florid syphilis may beget 
a healthy child. (2) By the mother (germ transmission), the father 
being healthy. The circumstances influencing the likelihood of infection 
are similar to those that obtain in the father; but a syphilitic woman 
almost always transmits the disease to her offspring, and this form of 
infection is much more fatal to the foetus than is the paternal, since 
not only is the ovum diseased, but also the source of nourishment of 
the foetus. A mother of a syphilitic child, though herself not obviously 
syphilitic, cannot become infected (having acquired an artificial im- 
munity), as is well expressed in Colles' law: A child born of a syphilitic- 
mother who is without obvious venereal symptoms, and which, with- 
out being exposed to any infection subsequent to its birth, shows this 
disease when a few weeks old, will infect the most healthy nurse, 
whether she suckle it, or merely handle and dress it; and yet this child 
is never known to infect its own mother, even though she suckle it while 
it has venereal * ulcers of the lips and tongue. (3) By both parents 
being syphilitic. This is very common, one parent having infected the 
other — in which event the likelihood of infection in the foetus is much 
enhanced. (4) By intra-uterine or placental transmission of the infection. 
A woman infected during pregnancy may, by way of placental trans- 
mission, infect her foetus; this is less likely to occur the older the foetus 
at the time of infection, and it is uncommon after the seventh month; 
but during birth the foetus may acquire the infection from vaginal 
lesions. 

A person having acquired syphilis is immune to a second infection, 
though occasional exceptions to this rule seem to be observed; and 
children who have inherited syphilis are immune to the acquired infec- 
tion (Prof eta's law). 

Pathology. — The primary lesion, or chancre, consists of serous and 
cellular infiltration (lymphoid, plasma, epithelioid, and occasionally 
giant cells), especially in the deeper layers of the skin or mucous mem- 
brane about the capillaries and small veins, together with proliferation 
of the vascular endothelium, thromboses of the small vessels, and 
hyperplastic and degenerative changes in the small nerves. Together 
these constitute a firm, hard, reddish papule — the hard chancre. Soon, 
on account of deficient blood supply (due to the thromboses), liquefac- 



182 PROTOZOAN INFECTIONS 

tion necrosis sets in, and this, involving the overlying and perhaps 
proliferated epithelium, leads to vesiculation and usually ulceration — 
the ulcer being circumscribed, " scooped out," and indurated at the 
base and about the edges. Ultimately the serous and cellular infiltration 
subsides and is removed; fibroblasts form and cicatrization ensues. The 
lymph nodes adjacent to the primary lesion, and later the other lymph 
nodes throughout the body, become enlarged and indurated (buboes), 
in consequence of serous infiltration and cellular proliferation, and 
those adjacent to the chancre sometimes undergo suppuration in con- 
sequence of secondary pyogenic infection. Later all the lymph nodes 
exhibit more or less well-marked sclerosis. The cutaneous and the 
mucous membrane lesions consist of proliferation and infiltration of the 
upper layers of the skin and the mucosa, in some cases associated with 
cellular infiltration of the rete Malpighii and proliferation of the underly- 
ing bloodvessels. The characteristic mucous patch (mouth, genitals, 
anus) and the similar condyloma (of the soft and usually moist skin of 
the perineum, groins, axillse, between the toes, etc.) exhibit lesions quite 
like those of the chancre — cellular infiltration of the deeper layers of 
the epithelium and elongation of the papillae, proceeding to necrosis 
and exfoliation of the superficial layers. Later in the course of the 
disease diffuse indurative changes occur in the bloodvessels (arterio- 
sclerosis, atheroma); these lead to or are associated with indurative 
changes in the organs (liver, spleen, kidneys, heart, brain, spinal cord, 
meninges, etc.). At the same time characteristic formations, so-called 
gummas (syphilomas, specific granulation tumors) appear, especially 
in the viscera, bones, periosteum, etc. These vary in size from so-called 
miliary gummas to formations ten to fifteen or more centimeters in 
diameter. They are firm, nodular, somewhat elastic, and on section 
gelatinous (or mucoid), and surrounded and pervaded by bands of 
dense, fibrous, connective tissue that also sends prolongations into the 
adjacent tissue. Occasionally considerable softening occurs, and if 
the gumma be situated in the skin or the mucous membrane small 
ulcers may form; these usually, sooner or later, cicatrize. Micro- 
scopically, the gumma consists of epithelioid and round cells and 
some giant cells, together with proliferation of the vascular endothelium, 
the formation of new bloodvessels, and a general tendency to sclerosis — 
although softening (mucoid and fatty degeneration) is quite common 
in the larger gummas. The so-called parasyphilitic lesions (syphilitic 
in origin but not in nature) exhibit no specific features. 

Symptoms of Acquired Syphilis. — The period of incubation varies 
from two to five weeks, being about three weeks in the majority of 
cases. Usually there are no prodromal symptoms, the first indication 
of the infection being the so-called hard, or Hunterian, chancre. This 
develops at the seat of inoculation — usually in men on the prepuce 
or glans penis, though sometimes in the urethra (where it may remain 
unobserved), and in women on the vulva, the vagina, or the cervix 
of the uterus. The chancre, however, may be extragenital — on the 



SYPHILIS 183 

anus, rectum, lips, tonsils, breast, ringer, etc. It consists of a firm, 
hard, painless, reddish papule, which soon exhibits slight central necrosis 
and ulceration, and may discharge a small amount of secretion, which 
sometimes dries to form a scab. By the third week the chancre has 
become characteristically hard, indurated, and cartilaginous; but this 
is more apparent on cutaneous than on mucous surfaces. At first it 
evinces no tendency to heal; but in most cases cicatrization is complete 
by the end of the fifth or sixth week, although it may be much delayed ; 
the scar, as a rule, remains indurated for a long time. During the 
second week the lymph nodes adjacent to the primary lesion (usually, 
therefore, the inguinal nodes) become enlarged, hard, and indurated 
(syphilitic bubo); they are painless unless secondary pyogenic infections 
leading to suppuration occur. By the end of the third or fourth week 
the lymph nodes in general (epitrochlear, axillary, cervical, auricular, 
submaxillary, etc.), are enlarged and indurated. 

The period prior to the development of the cutaneous and other 
so-called constitutional symptoms is usually spoken of as the primary 
stage, and lasts from six to twelve weeks. With the onset of the cutaneous 
manifestations the secondary stage is said to begin; this lasts from 
two months to a year or more, and is sometimes followed after a variable 
and uncertain period (often of apparently good health) by the so-called 
tertiary stage (gummas, certain cutaneous eruptions, amyloid degenera- 
tion, etc.); but no sharp line of demarcation between the secondary 
and the tertiary stage can be drawn: indeed, certain of the so-called 
tertiary manifestations sometimes develop unusually early, even before 
the chancre has healed. Nor is it correct to assume constitutional 
involvement only with the onset of the cutaneous and other manifesta- 
tions of the so-called secondary stage — constitutional involvement is 
effected even before the maturation of the chancre (treponemse may 
be demonstrated in the blood). 

General Symptoms. — Slight fever is not uncommon with the onset 
of glandular enlargement, and it is almost always present when the 
glandular enlargement has become universal. In other cases no note- 
worthy fever may be apparent until three or four weeks before, or 
concurrently with, the development of the cutaneous lesions. This 
" fever of invasion" (as well as the attacks of fever that may occur at 
any time during the secondary or tertiary stages) may be moderate 
(101° F.) or sometimes quite high (104° F. or more); and it may be 
continuous (when it is likely to be mild), or remittent (usually), or 
intermittent (when it may be accompanied by chilly sensations or chills). 
This fever may be mistaken for typhoid fever, malaria, tuberculosis, 
sepsis, rheumatism, etc. In addition to the fever, evidences of general 
infection are seen in malaise, languor, prostration, general neuro- 
muscular pains, bone pains (especially tibia, clavicle, and skull), joint 
pains, headache, iritis (exceedingly painful), coated tongue, poor 
appetite, slight enlargement of the spleen, and anemia (oligocythemia, 
disproportionate ologochromemia, and lymphocytosis). Late in the 



184 PROTOZOAN INFECTIONS 

disease aggravation of the anemia, cachexia, and amyloid degeneration 
may be observed. 

Cutaneous Lesions. — The cutaneous lesions (syphilides), usually 
looked upon as marking the beginning of the secondary stage, are 
characterized by their polymorphism, superficial character, general 
symmetry, copper-colored hue, and absence of itching. Erythematous, 
papular, pustular, squamous, and tubercular syphilides may be dis- 
tinguished. The commonest and the earliest is the roseola, which 
develops about eight to ten weeks after infection and consists of light 
reddish or rose-colored (later slightly coppery), roundish or ovoid macules, 
varying from 5 to 10 mm. in diameter, and irregularly distributed 
on the thorax and abdomen, sometimes on the thighs and arms 
(especially the flexor aspects), and rarely on the face. It persists for 
a week or two or longer; and may recur frequently. The syphilitic 
roseola may be accompanied, and is often followed, by papular and 
pustular syphilides, such as the so-called lenticulopapular, acneiform, 
varioliform, echthymaform, etc. These are usually distributed in 
groups over the trunk, flexor surfaces of the extremities, and the face, 
especially the forehead (corona veneris). A papulosquamous, so-called 
psoriasiform syphilide, is not uncommon; it may be circumscribed 
or widespread, and is rather common on the palms and soles. It may 
be distinguished from psoriasis by its coppery hue, absence of silvery 
scales, and absence of bleeding upon removing the scales. The soft 
and usually moist skin of the perineum, anus, vulva, groins, axillse, 
angles of the mouth, between the toes, etc., is often the seat of character- 
istic condylomas — flat, well-defined, wart-like growths. Concurrently 
with the roseola the hair usually becomes thinned, lustreless, and falls 
out (alopecia). It usually returns upon appropriate treatment, except 
in the event of ulceration and cicatrization, when the alopecia is perma- 
nent. Onychia and paronychia are rather common (more common 
in congenital syphilis), and often lead to brittleness and shedding of 
the nails. Late in the course of the disease different gummatous 
lesions of the skin occur, of which the lupiform syphilide and rupia are 
the most important — since they give rise to considerable ulceration 
and destruction of tissue. Small roundish or irregular whitish spots 
(leukoderma) also are sometimes observed, especially in women and 
about the neck; they are usually 2 to 5 mm. in diameter, but they may 
coalesce to form larger spots or bands (collier de Venus), or they may 
spread over a greater part of the body. 

Mucous Membrane Lesions. — The mucous membranes may be 
involved early or late, and the lesions may be erythematous, papular, 
ulcerative, or gummatous. Concurrently with the cutaneous rash, 
sometimes earlier, complaint is often made of sore throat, and on inspec- 
tion the pharyngeal, faucial, and tonsillar mucous membrane is found 
swollen, red, and hyperemic; small papules soon form, and the super- 
ficial epithelium becoming opaque and cloudy, and later ulcerated, 
gives rise to the characteristic mucous patch — a moist, whitish, flat, 









SYPHILIS 185 

superficial, somewhat raised, and well-defined area. Such mucous 
patches may be found on any mucous membrane or mucocutaneous 
junction of the body, although they are most common in the fauces, 
pharynx, uvula, cheek, tongue, lips, nose, larynx, anus, vagina, etc. 
Sometimes these patches coalesce or spread to form more or less extensive 
serpiginous ulcers, especially on the tonsil, uvula, soft palate, and 
pharynx. Hypertrophy of the papillae of the tongue is common early, 
and gives rise to papules which sometimes become necrotic and form 
small ulcers, especially near carious teeth; or ichthyosis may supervene; 
or the tongue may become atrophic, and the base, firm, hard, and smooth 
(Virchow's smooth atrophy of the base of the tongue) — which is of 
considerable diagnostic significance in persons over fifty years of age. 
Gummas are quite common in the mucous membranes and submucous 
tissues. In the tongue they not infrequently give rise to extensive 
ulceration and loss of tissue, and they have often been mistaken for 
carcinoma (and the tongue in consequence has been excised). 

Circulatory System. — The chief lesions consist of arteriosclerosis 
and its consequences, notably fibroid degeneration of the myocardium, 
aneurysm, and aortic valve disease, all of which are discussed under 
their respective headings. A special type of arteriosclerosis due to 
syphilis may be distinguished, and in the lesions, especially in the aorta, 
Treponema pallidum may be found. Occasionally a gumma forms in the 
myocardium, and if situated in the pathways of the bundle of His may 
give rise to heart block. Syphilitic endocarditis is very rare (aside from 
arteriosclerosis); syphilitic pericarditis is perhaps more common. 

Respiratory System. — The mucous membrane lesions in the nose 
(syphilitic rhinitis) have already been mentioned. In addition, gummas 
may occur, comparatively early. Usually they involve the bone before 
the mucous membrane; they give rise to considerable necrosis and 
destruction, to the occurrence of perforation of the hard and the soft 
palate and the bones and cartilages of the nose, and the consequent 
development of the so-called saddle nose and extreme fetor (ozcena). 
In the larynx, in addition to the common laryngitis, gummas may 
occur, and give rise to ulceration of the cartilages, with subsequent 
cicatrization and stricture. Involving first the epiglottis, they may 
cause a severe, even fatal, oedema of the glottis. Similar lesions may 
occur in the trachea or one of the main bronchi (dyspnoea, inspiratory 
stridor, lessened expansion and feebler breath sounds on the affected 
side); bronchial dilatation may occur below the site of the lesion. 
Syphilis of the lung is very rare : it may occur as small multiple gummas, 
about which there may be areas of bronchopneumonia; or it may lead to 
an interstitial fibrosis, developing, as a rule, from the root of the lung 
(perhaps very rarely from the pleura), and being especially conspicuous 
about the bronchi and the bloodvessels; the bronchi may become 
dilated. The diagnosis can rarely be made, although it may be sus- 
pected upon the development in a known syphilitic subject of the physical 
signs of chronic interstitial pneumonitis with bronchiectasis of the 



186 PROTOZOAN INFECTIONS 

lower lobe, and the absence of tubercle bacilli from the sputum; but 
one must remember that tuberculosis of the lungs may occur in a syphilitic 
subject, and tubercle bacilli may not be found for some time. A positive 
Wassermann reaction may be of diagnostic assistance. 

Digestive System. — Rarely a gumma may develop in the oesophagus 
and ultimately lead to stricture. An occasional syphilitic ulcer has 
been observed in the stomach, but otherwise syphilis of the gastro- 
intestinal tract is rare, except in the rectum. Gummas are quite common 
in the rectum, especially in women. They develop usually just above 
the internal sphincter, and, gradually cicatrizing, produce a stricture. 
The symptoms are those of gradually increasing difficulty in evacuating 
the bowels and narrowing of the fecal masses. The stricture may be 
recognized by palpation and protoscopic examination, and may be 
distinguished from carcinoma by its being firm and fibrous rather 
than a more or less exuberant, centrally ulcerated mass, and by the 
absence of the carcinomatous cachexia. 

Syphilis of the liver is very common. Jaundice is not uncommon 
at the time of development of the cutaneous rash and enlargement 
of the lymph nodes; it is likely due to radicular cholangitis. Some- 
times a type of acute yellow atrophy supervenes. In the tertiary stage, 
the lesions may consist of: (1) Gummas, which may be single or 
multiple; usually they give rise to a large protruding tumor in or near 
the epigastrium, together with local pain and distress. The diagnosis 
is facilitated by the detection of evidences of syphilis elsewhere. Carci- 
noma may be eliminated by the less rapid growth or stationary condition 
of the enlargement (growth is usually rapid and progressive in car- 
cinoma), and by the absence of the general, cachectic, manifestations 
of carcinoma. In some cases, however, the therapeutic test is necessary 
to establish the diagnosis. The presence of fever may suggest liver 
abscess, but the other evidences of suppuration are usually absent. 
Following absorption of the gumma the liver becomes more or less 
distorted from scar formation. (2) Chronic interstitial hepatitis. These 
cases exhibit the common manifestations of cirrhosis — enlargement 
of the liver with the signs of portal obstruction and ascites; there is 
likely to be also slight jaundice and some fever, at least from time to 
time; later the liver may decrease in size. Perihepatitis is usually asso- 
ciated, and may give rise to palpable and audible frictions. The lesions 
may also implicate the peritoneum more extensively. (3) Amyloid dis- 
ease presents the symptoms and signs mentioned under amyloidosis. 

Genitourinary System. — In a few cases an acute syphilitic nephritis 
occurs during the second stage of the disease; death may ensue soon, 
but, as a rule, recovery follows after a number of months, although 
albuminuria may persist for a long time. A chronic parenchymatous 
nephritis may be associated with the renal and other lesions of amy- 
loidosis. Chronic diffuse indurative (or interstitial) nephritis is a 
common sequence of syphilis and the arteriosclerotic changes that it 
induces. Miliary or larger gummas may be found in the kidney, espe- 



SYPHILIS 187 

cially in association with syphilis of the liver. The testicle may become 
the seat of gummas or of progressive fibrosis (interstitial orchitis). 
Abortion and repeated abortion is common in syphilitic women. 

Nervous System. — The lesions of the brain may consist of: (1) 
Syphilitic arteriosclerosis, which may lead to aneurysm and rupture 
of a vessel (apoplexy), or to thrombosis and cerebral softening. (2) 
Gummas, which may be single or multiple, and vary in size from that 
of a pea to that of an egg. They may occur in any part of the brain, 
but usually develop in the dura mater or the pia-arachnoid at the base 
of the cerebral hemispheres, near the pituitary body, or on the convexity 
of the frontal convolutions. When the meninges are involved, a sub- 
acute or chronic meningitis with much thickening results, and the 
lesions are likely to extend along the nerve sheaths (especially the 
oculomotor, the facial, etc.). The symptoms of the larger gummas 
are those of tumor of the brain — especially headache, vomiting, con- 
vulsions, optic neuritis, etc., together with various localizing symptoms 
depending upon the situation of the gumma. (3) Meningitis — which 
may occur without definite macroscopic gummatous formations, although 
microscopic gummas are almost always present. This is common 
at the base of the brain, where it usually implicates one or more of the 
cranial nerves, especially the oculomotor, the trochlear, the abducens, 
and the trigeminal; but it may involve also the cortex. The chief 
symptoms consist of initial headache, which may be local or general, 
and constant or intermittent, but is usually worse at night; vertigo, 
somnolence, failure of mentality, mental depression, sometimes irri- 
tability, and localizing symptoms depending upon the cranial nerves 
involved. In some cases there is eventually coma or convulsions ; rarely 
these may be the major initial manifestations. The symptoms due to 
cortical involvement are those of meningo-encephalitis, which gradually 
progress to well-defined paretic dementia. 

Spinal cord lesions are less common than cerebral; they may consist 
of arterial disease (with softening of the cord); or gumma (tumor for- 
mation) of the meninges or the cord; or meningitis (which usually is 
irregularly distributed, although it involves all the meninges and the 
spinal cord and the spinal nerve roots); or of myelitis and secondary 
sclerosis. The so-called parasyphilitic (metasyphilitic) diseases involve 
the nervous system, and consist of tabes dorsalis, paretic dementia, 
etc. The diagnosis of cerebrospinal syphilis, in some cases readily 
made, may be difficult; the symptoms are likely to be variable, multi- 
form, and asymmetrical, to exhibit combinations of spinal, cerebral, 
and meningeal symptoms not readily explainable by a single or well- 
defined lesion. In some cases resort must be had to antisyphilitic 
treatment to settle the diagnosis. 

The Bones, Joints, Burs^e, and Muscles. — Syphilitic periostitis 
is common, and gives rise to local pain, often worse at night, tenderness, 
and swelling. Gummas may develop in the periosteum as well as 
in the deeper structures, reaching even to the medulla and causing 



188 PROTOZOAN INFECTIONS 

considerable destruction. Occasionally acute or chronic synovitis is 
observed; or a syphilitic osteo-arthritis may occur. The muscles may 
be the seat of an early myositis, or of a later gummatous formation. 
Absorption of the gumma may lead to more or less loss of substance 
and fibrosis. The syphilitic bursopathy of Verneuil, occurring especially 
about the larger joints (knee, elbow, etc.), is a rare manifestation. 

Symptoms of Congenital Syphilis. — Aside from the primary sore, 
congenital syphilis presents all the manifestations of the acquired 
disease. The child at birth may present obvious evidences of the 
disease, or it may appear healthy, the symptoms not developing until 
about the second month; in other cases, the symptoms first become 
obtrusive about puberty (delayed congenital syphilis). The infant 
obviously syphilitic at birth is poorly nourished, wizened, old-looking; 
it suffers from coryza that interferes with respiration (whence "snuffles") 
and with suckling; the lips and the angles of the mouth are fissured 
and ulcerated, and blisters are present on the hands, wrists, feet, and 
ankles (pemphigus neonatorum). The liver, spleen, and pancreas 
are usually enlarged; the lungs are heavy, firm, grayish white, and 
almost, if not quite, airless (the so-called white pneumonia of Virchow); 
and the ends of the long bones commonly reveal an osteochondritis 
that may lead to separation of the epiphyses. Hemorrhages, sub- 
cutaneous, submucous, umbilical, occur in some cases. These infants, 
as a rule, soon die; foetuses born dead reveal the same changes. 

In other cases the infant is apparently healthy at birth. Usually 
early in the second month the syphilitic rhinitis ("snuffles") develops; 
the discharge may be serous, or purulent, or sanguinolent, and is highly 
infectious. Necrosis and ulceration of the nasal bones and cartilages 
may ensue, and lead to falling in of the nose — the so-called saddle- 
nose; or the lesions may spread to the pharynx, the Eustachian tube, 
and the middle ear, and give rise to otorrhcea and deafness. Cutaneous 
lesions quite analogous to those of the acquired disease develop ; usually 
they begin about the genitals and buttocks, but tend to spread over the 
body. The most common is a yellowish or reddish-brown erythema, 
but the lesions may be also papular, eczematous, or pustular. Fissures 
(ragades) are common about the lips, especially at the angles of the 
mouth. Mucous patches, condylomas, alopecia, onychia, dactylitis, 
iritis, etc., also occur; the liver and spleen are usually enlarged; 
the bones about the fontanelle and elsewhere may be thickened, and 
the epiphyses may be enlarged. Many of these children also die; but 
in favorable cases and under appropriate treatment, the symptoms 
subside toward the end of the first year, and the child may appear 
perfectly healthy until about puberty. From puberty to about the 
twentieth year many so-called late manifestations of congenital syphilis 
occur. As a rule, growth is retarded, and the child appears wizened 
and prematurely old; the skull may be large or asymmetrical, the 
nose depressed, the lips prominent, and scars of healed fissures may 
radiate from the corners of the mouth — appearances which of them- 






SYPHILIS 189 

selves suggest the disease. The teeth are likely to be deformed, and 
the two upper central incisors may be short and broad, peg-shaped 
(narrower below than above), and reveal a single notch at the free edge 
(Hutchison's teeth). Interstitial keratitis (ground glass opacity of 
the cornea), usually bilateral, and bilateral deafness, unassociated with 
pain or discharge, are quite common. The malformations of the 
teeth, interstitial keratitis, and deafness constitute Hutchison's triad 
of congenital syphilis. Bone lesions also are common — especially 
bilateral gummatous periostitis, affecting especially the tibiae, but also 
other bones, and leading to permanent thickenings and deformities. 
Joint lesions are rare, although a synovitis, usually symmetrical and 
involving the knee by preference, may occur. Gummas in different 
parts of the body and amyloid disease are rare manifestations. 

Diagnosis. — In some cases the initial lesion is so characteristic 
as to admit of no doubt of the diagnosis; in other cases in the past, 
certainty was not obtainable until the development of enlarged lymph 
nodes and the cutaneous rashes. But at present Treponema pallidum 
may be readily demonstrated in the serum of the chancre (by "dark- 
field" illumination or by staining), as well as in a section excised from 
the chancre, and in the circulating blood, so that it is no longer necessary 
to await the tedious appearance of the so-called secondaries to make a 
positive diagnosis and institute treatment. In older cases in which 
the diagnosis is uncertain, aid may be obtained by a history of a primary 
lesion or of exposure to infection, but both may be denied; there may 
be, however, a history of sore throat, cutaneous rashes, alopecia or 
iritis, etc., and in women of repeated abortions; search may reveal 
the scar of a primary lesion or of other syphilitic lesions elsewhere, 
or copper-colored cicatrices on the legs (not always syphilitic), or peri- 
osteal thickenings, or enlarged lymph nodes, etc. Congenital syphilis 
in early infancy is readily recognized from the general appearance of 
the child, the snuffles, the cutaneous eruptions, the ragades at the angles 
of the mouth, the condylomas, enlarged liver and spleen, etc. Snuffles 
and a rash occurring within the first three months of life are almost 
certainly syphilitic. There may be also a history of syphilis in one or 
both parents. The disease manifesting itself about puberty may be 
recognized by the retarded growth and general appearance of the 
child, Hutchison's teeth, usually bilateral keratitis, bilateral deafness, 
symmetrical nodosities on the bones, etc. In any case of supposed 
congenital or acquired syphilis, or of parasyphilitic disease, such as 
tabes dorsalis, paretic dementia, arteriosclerosis, aortic valvular disease 
of the heart, etc., resort may be had to the TVassermann reaction, which 
seems to give positive results in 80 to 90 per cent, of the cases. Finally, 
in doubtful cases, resort may be had to the therapeutic test, which, 
however, is by no means infallible. 

Prognosis. — In acquired syphilis, the outlook is good if treatment 
is instituted early and carried out efficiently and for a sufficiently 
long time — which is rarely the case. Some cases are unusually virulent, 



190 PROTOZOAN , INFECTIONS 

and more or less rebellious to treatment; and in other cases a fatal 
acute yellow atrophy of the liver may supervene. Death is frequently 
due to tertiary, gummatous lesions, and to related disorders due to 
arteriosclerosis, etc. The prognosis in the parasyphilitic diseases, tabes 
dorsalis and paretic dementia, is almost hopeless as to cure. Congenital 
syphilis may lead to death of the foetus or to death soon after birth, 
hemorrhages, jaundice, and pemphigus especially being bad omens. 
The ocular and aural manifestations developing about puberty may 
be more or less permanent. There is considerable doubt whether 
syphilis can be transmitted to the third generation. 

Treatment. — The only efficient method of prophylaxis is to avoid 
the sources of infection. A syphilitic subject should be told of the 
danger of transmitting the disease by kissing, for instance, as well as 
by contaminating any article that he may use, such as table utensils, 
pipes, public drinking vessels, personal and bed linen, towels, etc. 
Physicians, nurses, midwives, barbers, chiropodists, etc., should 
carefully sterilize all instruments, towels, etc., that have been used 
on known or supposedly syphilitic persons. A syphilitic infant 
may be nursed by its mother, but should not be given to a healthy wet 
nurse, who certainly would acquire the infection from the infant. From 
a purely medical point of view, altogether aside from the question of 
morals involved in exposing an innocent and unsuspecting woman 
and possible children to the likelihood of infection, a syphilitic subject 
must not marry until at least four years have elapsed since infection; 
the first two years must have been devoted to persistent and efficient 
treatment, and during the second two years the subject must have been 
entirely free from symptoms; otherwise the physician must prohibit 
the marriage, and such quasi approval as he may give should be always 
reserved, since even after apparently efficient treatment infection may 
be transmitted, and late results, such as gummas, tabes dorsalis, and 
paretic dementia, are likely to ens,ue. 

Opinions differ as to the propriety of excising the initial lesion with 
a view to prevent constitutional symptoms. Although it is undoubtedly 
true that general infection has occurred by the time the chancre has 
matured, it is perhaps possible to minimize the infection by early remov- 
ing the main hatching ground; this, however, can scarcely be proved, 
although it has been successful in the ape. Treponema pallidum, how- 
ever, should first be demonstrated in the chancrous discharge. If not 
removed, the chancre should be washed with an antiseptic solution, such 
as mercuric bichloride 1 to 2000, and dusted with calomel; or a calomel 
ointment (10 per cent.), or mercurial plaster, may be applied. 

Internal medication should be commenced as soon as the diagnosis 
is certain, and not sooner. If Treponema pallidum has been early iden- 
tified, treatment may then be instituted; otherwise, one should await the 
general lymph-node enlargement, the cutaneous rash, and other so- 
called secondaries. Mercury is the sovereign remedy, and may be 
given by the mouth, by inunction, by intramuscular injection, and 






SYPHILIS 191 

bv fumigation. The preferable preparations for administration by the 
mouth are: Mercury with chalk (containing 38 per cent, of mercury), 
which may be given in doses of 1 grain (0.06 gram), with or without 
an equal amount of Dover's powder to prevent diarrhoea in those sus- 
ceptible; the protoiodide (J grain, 0.015 gram), the tannate (J grain, 
0.015 gram), and the biniodide (yg grain, 0.004 gram), three times a 
day. The dose may be increased to the point of toleration (abdominal 
pain, diarrhoea, tenderness of the gums), whereupon the dosage should 
be reduced one-half, and continued thereat for one year, provided the 
general health of the patient is maintained. Should the general health 
fail, the mercury should be stopped, and iron and tonics substituted. 
Should relapses occur while taking the mercury, the dose should be 
increased, or another method of administration resorted to. During 
the second year, in the absence of symptoms, there should be alternating 
periods of treatment and of cessation of treatment of a month or six 
weeks each; if symptoms are present, treatment should be continuous, 
as in the first year, and the alternate periods of treatment and cessation 
thereof should be resorted to in the third year. 

In cases in which a rapid influence is desired, inunctions may be 
resorted to. After preliminary cleansing, 1 dram (4 grams) of the 
official mercurial ointment (50 per cent, of mercury), or an equivalent 
amount of the oleate (10 per cent, of mercury), should be rubbed into 
the body daily (for 20 to 30 minutes) on six consecutive days; on the 
seventh day the patient should have a warm, cleansing bath. The 
skin of the parts selected for the inunction should be thin and as free 
from hair as possible: the inner aspect of the thighs, the sides of the 
chest and abdomen, and the arms are six serviceable regions that may 
be used in rotation. ^Yhen the inunction is done by some one other 
than the patient, the rubber should be protected by gloves or he should 
use a glass rod or spatula. The treatment should be continued for four 
or five weeks, and then discontinued; but at least two courses of such 
treatment should be given yearly for two years, or longer should symp- 
toms recur. Intramuscular injections are exceedingly valuable in 
intractable cases, in cerebrospinal syphilis, and in persons who dislike 
the inconvenience and publicity of pills and inunctions. One may 
use: (1) The insoluble salts of mercury, such as calomel, 1 grain 
(0.06 gram), in 15 minims (1 c.c.) of sterile olive oil; gray oil, 1 to 2 
minims (0.06 to 0.12 c.c.) diluted with olive oil; or mercury salicylate, 
10 minims (0.60 c.c.) of a 10 per cent, suspension in paraffin oil; or 
(2) the soluble salts of mercury, of which the bichloride is the best, 
and may be used in doses of -J grain (0.008 gram) in 15 minims (1 c.c.) 
of sterile physiological saline solution. The injections should be made 
deep into the buttock, in the centre of a line running from the anterior 
superior spine of the ileum to the upper end of the intergluteal fold. 
The insoluble salts should be injected once a week for twelve to fifteen 
weeks, and the soluble salts, at first daily, then every other day, and 
then twice a week until about forty injections have been made. The 



192 PROTOZOAN INFECTIONS 

injections may then be discontinued for a month of two, but, as in the 
other methods, treatment must be resorted to for shorter periods for at 
least two years, and again if any symptoms recur. 

In the late or tertiary stage of the disease (visceral and bone lesions) 
the iodides should be given, either alone or alternating with or in combi- 
nation with mercury (so-called mixed treatment). The iodide may be 
given in gradually ascending doses, in some alkaline water or milk; 
although excellent results sometimes attend the use of small doses, 15 
grains (1 gram) daily, it is wise, as a rule, to give large doses to the 
point of toleration (150 grains, 10 grams, or more a day). One may give 
the iodide and mercury together, as in the following prescription (the 
arsenic has been added for its tonic effect and to prevent acne, coryza, 
and other manifestations of iodism, but it may be omitted): 



i^ — Mercuric bichloride 1 grain 6 

Potassium iodide 3 drams 12 

Solution of potassium arsenite 30 minims 2 

Compound syrup of sarsaparilla 4 ounces 120 

Water sufficient to make 8 ounces 250 

Sig. — One tablespoonful (15 c.c.) in water three times a day. 





0— M. 



The iodides should be continued for two or three months, then inter- 
mitted for a month, and then resumed, alternating thus month by month 
for a year. Mercury is sometimes administered also by fumigation 
(sublimation of calomel), and, rarely, by intravenous injection. At all 
times when mercury is being taken the greatest care must be exercised 
to keep the mouth clean, by frequent use of the toothbrush, and of 
solutions of potassium chlorate or mild antiseptics. Alcohol and 
tobacco should be interdicted. Mucous patches may be treated with 
solid silver nitrate, acid nitrate of mercury, etc.; condylomas about 
the genitalia by cleansing with mercuric bichloride, 1 to 2000, and 
dusting with calomel; scaly lesions on the hands, feet, etc., by a 10 
per cent, ointment of ammoniated mercury; and ulcerating cutaneous 
gummatous lesions by cleansing and the application of mercurial plaster. 
The syphilitic cachexia should be treated with bitter tonics, iron, quinine, 
strychnine, syrup of iron iodide, cod-liver oil, arsenic, the lactophosphates, 
and hypophosphites. 

Syphilitic infants are best treated with mercurial ointment (diluted 
with an equal part of vaseline) or the oleate of mercury on the binder, 
or by administering mercury and chalk, J grain (0.03 gram), three 
times a day. The later lesions occurring about puberty may be treated 
with mercury and the iodides, the following formula being serviceable: 

3$ — Mercuric bichloride J^ grain 03 

Potassium iodide 1H drams 6 

Tincture of iron chloride 2 drams 8 

Syrup of lemon 2 ounces 60 !0 

Water sufficient to make 4 ounces 120 '0 — M. 

Sig. — One teaspoonful (5 c.c.) in water three times a day. 



YAWS 193 

YAWS. 

(Framboesia.) 

Yaws is a chronic, infectious, and highly contagious disease, caused 
by Treponema pertenuis (Castellani), and characterized by a papular 
rash which usually develops into a f ungating, granulomatous, encrusted 
eruption. 

Etiology. — Yaws is widely distributed throughout the tropics, espe- 
cially Africa, Asia, Central and South America, the Pacific Islands, 
and the West Indies. During the early part of the nineteenth century 
it was exceedingly common among the slaves of our southern countries, 
but has now practically disappeared from the land. The disease 
attacks persons of all ages, but children are most susceptible. Indeed, 
in some parts of the West Indies and in Fiji nearly every child is attacked, 
and those who might otherwise escape are often voluntarily exposed to 
infection by their parents under the impression that the disease is a 
necessary part of a child's training. The black and the yellow races 
are more susceptible than the white. One attack seems to confer partial 
immunity. The disease is not hereditary or congenital, as is syphilis, 
for which it is sometimes mistaken. 

The exciting cause of the disease is Treponema pertenuis. The disease 
is highly contagious. The contagium may be transmitted directly, that 
is, from the sick directly to the well; by means of fomites, such as articles 
of domestic use, dishes, etc.; and probably also by insects; but an open 
wound or abrasion seems requisite for infection. Mere residence in an 
infected locality (a house, for instance) seems to have sufficed for infec- 
tion, but many other factors must be considered in such cases. The 
infection is inoculable into lower animals, such as the monkey. 

Symptoms. — The period of incubation varies from about two weeks 
(in inoculation cases) to as much as six months (in cases otherwise 
acquired). Prodromal symptoms are usually absent, though there may 
be for several days malaise, headache, fever, and vague neuromuscular 
pains. The disease begins, certainly in the inoculation cases, and usually 
also in other cases, with the development of a papule at the site of inocula- 
tion — usually on the feet, legs, or face. At the end of a week this 
is converted into an ulcer, which at the end of another week heals and 
leaves a superficial cicatrix. This is called the primary eruption or sore. 
The secondary eruption, w T hich may occur with the primary eruption, 
or be delayed for two weeks, consists of pin-sized papules which gradually 
increase in size until they reach that of a pea or a small nut, or, by conflu- 
ence, that of a small apple. They may be distributed more or less 
widely over the body, but are found most commonly at or about the muco- 
cutaneous junctions and on the limbs, neck, and trunk; the hairy scalp 
and the axilla are rarely involved. They consist largely of granulation 
tissue and inflammatory overgrowth of the papillary layer of the cutis 
and the Malpighian layer of the epidermis. They much resemble 
13 



194 PROTOZOAN INFECTIONS 

syphilitic condylomas, and itch considerably, but are otherwise painless. 
Their epidermic covering becomes thinner, and is ruptured or shed, 
permitting the escape of a whitish-yellow, seropurulent fluid which dries 
and forms crusts, which are usually quite tough, often very hard, and 
adherent. When removed they reveal irregular, reddish granulation 
tissue, which has been likened to a raspberry, whence the name fram- 
bcesia (frambcesia, raspberry). The yaw, as a rule, reaches its maximum 
development in about two weeks, remains stationary for about two 
weeks, and then begins to shrink. The crust dries up, the papillomatous- 
looking granulation tissue is gradually converted into a cicatrix, which 
is pale in the negro, pigmented in the white race, and surrounded by an 
area of increased pigmentation. 

In some cases the primary eruption is followed by one or more 
relapses, associated with fever and severe neuromuscular pains in the 
back. In other cases the yaw itself ulcerates, but may heal after a 
time with considerable cicatricial contraction. 

Diagnosis. — The disease is commonly unmistakable, but care must 
be exercised to exclude syphilis, verruga, leprosy, tuberculosis, and 
epithelioma. Treponema pertenuis may be demonstrated in the lesions, 
especially the papillomatous skin lesions. 

Prognosis. — The duration of yaws is from a few weeks to several years. 
In most cases recovery ensues. Young children, however, and older 
persons the subject of divers constitutional diseases, may succumb. 

Treatment. — Attention to general hygienic measures is imperative — 
isolation, fresh air, good food, suitable clothing (to obviate cold and 
chill), and daily warm baths. The ulcerated areas should be treated 
antiseptically and with stimulants, such as copper sulphate, silver nitrate, 
chromic acid, etc. Potassium iodide internally is believed to be of much 
value in effecting the disappearance of the local lesions. Mercury 
is sometimes used, but often avoided, as tending to do harm. The 
bitter tonics and iron, arsenic, and quinine are useful as general 
measures. 

TRYPANOSOMIASIS. 

(Sleeping Sickness; African Lethargy; Tsetse Fly Disease.) 

Trypanosomiasis is a chronic, specific, infectious disease caused by 
Trypanosoma gambiense, and characterized by fever, weakness, lassitude, 
emaciation, and eventually by protracted lethargy — sleeping sickness. 

Etiology. — Sleeping sickness is known to have existed for the last one 
hundred years on the west coast of Africa, and recently has been reported 
inland. It affects the white as well as the colored race, and it is common 
at all seasons. The specific exciting cause is Trypanosoma gambiense, 
which is transmitted by a tsetse fly, Glossina palpalis, which Koch 
believes becomes infected by feeding on infected crocodiles, and which 
probably serves as an alternate host; that is, the parasite probably under- 
goes some phase of development in the fly. 



KALA-AZAR 195 

Symptoms. — The period of incubation is probably from two to three 
weeks. In the early stage of the disease, which varies in duration from 
about three to as much as three years, the only symptom of marked con- 
stancy is enlargement of the lymph nodes, but there may be also irregular 
fever, rapid pulse, mental hebetude, slight anemia, and some loss of 
weight. This stage gradually merges into the second stage, that of 
sleeping sickness. The patient becomes definitely dull, listless, and 
apathetic; the pulse becomes rapid (120 or more per minute) and weak; 
the temperature becomes irregular, often rising as high as 101° or 102° in 
the evening; indefinite pains are complained of in the head and through- 
out the body; patches of erythema or of oedema may develop on the skin. 
There is gradual loss of strength in the arms and legs, associated with 
tremors, as well as with tremors of the tongue. The patient lies most of 
the time in a lethargic state and becomes emaciated. Finally, during 
the last two or three weeks of life the temperature falls below normal, 
and the patient ultimately dies in coma. 

Diagnosis. — The diagnosis may be made tentatively from a considera- 
tion of the symptomatology and possible etiological factors, and positively 
on finding Trypanosoma gambiense in the enlarged lymph nodes 
(aspiration of some fluid therefrom with a hypodermic needle and syringe), 
circulating blood, or cerebrospinal fluid. Darling has described, as 
occurring upon the Isthmus of Panama, a fatal infection resembling kala- 
azar, that he has named Histoplasma capsulatum, and due, as he 
believes, to an organism resembling Leishmania donovani. 

Prognosis. — The disease is invariably fatal. 

Treatment. — Prime importance must be attached to avoiding the 
tsetse fly, and searching out and destroying its breeding places. Treat- 
ment is unavailing, arsenic being the only drug apparently capable of 
producing any good effects, and it only prolongs life. The ordinary 
preparations or atoxyl may be used. They have sometimes been com- 
bined with aniline preparations, such as trypanroth, with asserted good 
results. Hopes are entertained of the production of an efficient serum. 



KALA-AZAR. 

(Tropical Splenomegaly; Tropical Cachexia; Dum-dum Fever; Piroplasmosis .) 

Kala-azar is a chronic, specific, infectious disease caused by Leishmania 
donovani, and characterized by intermittent or remittent fever, marked 
and progressive anemia and emaciation and enlargement of the spleen 
and the liver. A similar organism, described as Leishmania infantum 
(Pianese and Nicolle), has been found in certain types of infantile splenic 
anemia. 

Etiology. — Kala-azar was formerly believed to be indigenous in the 
lowlands of India, but it is now known to occur in many regions of the 
Orient. How the disease is transmitted is not definitely known. Patton 
has studied the flagellated stage of Leishmania donovani in the bed-bug 



196 PROTOZOAN INFECTIONS 

(Cimex rotundatus), but whether this is a transmitting agent has not yet 
been determined. 

Symptoms. — The period of incubation is not definitely known, but it 
may be less than ten days (Manson). The onset of the disease is usually 
abrupt — chills, fever (104° to 106°), vomiting, and rapid enlargement of 
the spleen and liver. The fever, though somewhat irregular in type, 
remains high for a few days to six weeks, and then subsides by lysis to 
normal or subnormal ; recurrences are common, and a low grade contin- 
ued fever may supervene. Profound debility, emaciation, and anemia 
(rarely less than 2,500,000 erythrocytes) and marked leukopenia (involving 
especially the polynuclear neutrophiles) ensue. The skin becomes pecu- 
liarly pigmented— of an earthy gray or drab color; and subcutaneous 
hemorrhages and dropsical effusions may develop in the skin and the 
serous sacs. The disease lasts for several months, as a rule, but may 
be prolonged to one or even two years. 

Diagnosis. — The diagnosis is suggested by continued fever, enlarge- 
ment of the spleen, leukopenia (relative lymphocytosis), and is con- 
firmed by detecting Leishmani donovani in the blood (especially in the 
leukocytes) or in the tissues. 

Prognosis. — Death occurs in about 96 per cent, of the cases — from 
exhaustion, or intercurrent infections, such as chronic diarrhoea, etc. 

Treatment. — The treatment is purely hygienic, dietetic, and sympto- 
matic. Removal from infected regions and isolation of the patient are 
advisable. 

ORIENTAL SORE. 

(Tropical Ulcer; Delhi Boil.) 

Oriental sore is a chronic, specific, granuloma that occurs endemically 
in certain tropical and subtropical countries, is caused by Leishmania 
tropica (Helcosoma tropicum, Wright), and is characterized by a nodule, 
which breaks down and forms an indolent ulcer. 

Etiology. — How the exciting cause of the disease is transmitted is 
not known, but the bite of an insect or infection of an already existing 
wound is usually postulated. Age, sex, race, and occupation are devoid 
of etiological significance. One attack seems to confer immunity. 

Symptoms. — The disease begins with a small, red spot, resembling 
a mosquito bite, in the centre of which a small nodule or papule soon 
forms. The surface becomes covered with fine scales that form a crust, 
Which, when removed or separated spontaneously, leaves a shallow, 
painless ulcer, that may itch considerably. About this similar ulcers 
develop, and by coalescence of many, a single ulcer, often an inch in 
diameter, results. In some cases there is only one, sometimes two ulcers, 
whereas in other cases there may be as many as twenty. After the lapse 
of from two to twelve months, healing begins. The resulting cicatrix 
may occasion considerable deformity, especially if on the face. Occa- 
sionally the nodule does not ulcerate, but merely desquamates at the 



MALARIAL INFECTIONS 197 

end of several months. The general health is little, if at all, disturbed. 
Enlargement of the lymph nodes, lymphangitis, phlebitis, erysipelas, 
abscesses, and gangrene are sometimes encountered as complications, 
and may result in death. 

Diagnosis. — The diagnosis suggested by the symptoms, is confirmed 
by detecting the specific cause. 

Prognosis.— The specific lesion itself rarely leads directly to death, 
but the prognosis as to cure is unfavorable. 

Treatment. — Cauterization of the specific lesion is recommended by 
some observers. At all events it should be dressed antiseptically. 
Change of climate and tonics are said to be useful in some cases. 



MALARIAL INFECTIONS. 

(Ague; Intermittent Fever; Remittent Fever; Pernicious Remittent Fever; Bilious 

Remittent Fever; Estivo-autumnal Fever; Paludism; Swamp Fever; 

Marsh Fever.) 

The malarial infections comprise a group of specific infectious dis- 
eases, caused by Plasmodium malaria? (Haemamceba malarise, Laveran), 
and variously characterized by intermittent or remittent fever, enlarge- 
ment of the spleen, the presence of the specific microorganism in the 
circulating blood, and sometimes by certain so-called pernicious mani- 
festations or a chronic cachexia. 

Etiology. — The malarial infections are widely disseminated throughout 
all parts of the world. Though especially prevalent in tropical and sub- 
tropical regions, they frequently prevail extensively in the temperate 
zones; but a noteworthy diminution in the prevalence of the infections 
is found to follow intelligent agricultural pursuits, efficient drainage, and 
other sanitary measures commonly introduced by the more enlightened 
people. On the contrary, the infections not infrequently break out 
among laborers engaged in constructing railroads, canals, fortifications, 
and other operations connected with upturning the soil. These and 
other etiological (telluric and atmospheric) factors, such as comparatively 
high atmospheric temperature and humidity, are of influence only in 
so far as they favor the growth and development of the Anopheles mos- 
quito — the essential factor in disseminating the infections. The mos- 
quito fructifies and flourishes best at a temperature of 75° F., or over 
— whence the malarial infections are most common in tropical and sub- 
tropical regions, and in temperate zones during the summer. Pools of 
stagnant water are essential for the breeding of mosquitoes — whence 
malarial infections are common in the neighborhood of earth-cutting 
operations accompanied by the formation of holes and surface irregular- 
ities wherein water collects and stagnates, and in the neighborhood of 
low marsh lands, swamps, and old river beds, where the water affords 
the necessary medium and the abundant vegetation additional protection 
for the developing larvae. The malarial infections are less common at 



198 PROTOZOAN INFECTIONS 

high than at low altitudes, because the mosquitoes, as a rule, do not 
fly high; nor do they fly far (200 to 300 yards), although they may be 
carried long distances by winds; and the proverbial insalubriousness of 
the night air is attributable to the fact that the malaria-bearing mosquito 
(Anopheles) peregrinates only at night. 

In this country the malarial infections at present are endemic along 
the Gulf of Mexico and the Mississippi River and in the States adjacent 
thereto, and they are rather common in the Middle and Southern States 
that border the Atlantic Ocean. They are much less common than 
formerly in the central, New England, and Northwestern States ; and the 
Hudson, the Delaware, and the Schuylkill valleys, formerly much in- 
fected, are now comparatively free. The infections are uncommon in 
Canada. Many of the Central and South American States, especially 
those along the coasts, are markedly infected. The British Isles are 
practically uninfected. The valleys of lower Russia, the Balkan prov- 
inces, Italy, and India present many foci of infection, and along the 
coast of Africa the most malignant forms of the infections are endemic. 

Age, sex, and race are devoid of etiological significance. The sup- 
posed relative immunity of the adult negro of South Africa has been 
found to be due to a relative immunity acquired during childhood, when 
the disease is very common, though often masked. Occupation is of 
significance only in that laborers on railroads, in swamps, etc., and 
soldiers, fishermen, farmers, etc., are more exposed to the likelihood of 
being bitten by infected mosquitoes. 

The essential etiological factor, then, is infected mosquitoes. Thus far 
only mosquitoes of the genus Anophelinse have been found to be malaria- 
bearing hosts, and of the one hundred and fifty or more species, forty 
have been proved by experiment to be active infectious agents. The most 
common and important are: Anopheles maculipennis (also called quad- 
rimaculatus, and claviger — the most common), Anopheles punctipennis, 
Anopheles crucians, and Anopheles argyritarsis. Fortunately in the 
temperate zone the common mosquito is not Anopheles, but Culex — 
which does not transmit malaria (though it does transmit filarial disease). 
The two may be distinguished by the fact that the palpi of the adult Culex 
are very short, while those of Anopheles are almost if not quite as long 
as the proboscis; the wings of Anopheles are distinctly mottled (brownish), 
while those of Culex are not (aside from the veins) ; Culex while resting 
has its body nearly parallel with the surface (wall) and its posterior 
pair of legs turned up over its back, while Anopheles rests with its body 
almost at right angles (45 degrees or more) to the wall and its posterior pair 
of legs usually against the wall or hanging downward. Anopheles is 
a rural insect, breeding especially in shallow pools, irrigating ditches, 
and the still edges of running streams, often remote from human habita- 
tions; Culex is a city beast, breeding in tanks, cisterns, and stagnant 
pools of water near or in houses. The males of all mosquitoes have 
feathered antennae (woolly heads), while the females have not. 

The mosquito, like other insects, passes through the stages of ovum, 



MALARIAL INFECTIONS 199 

larva, pupa, and imago (adult insect). Depending upon the genus, 
and the environmental conditions, such as season, temperature, stillness 
of the water, food, etc., the cycle of development from ovum to imago 
takes from ten days to three or four weeks. The male mosquito thrives 
on the juices of plants, whereas the female mosquito feeds mostly upon 
the blood of vertebrates, a meal of which is said to be essential to the 
deposition of eggs. These, as a rule, are deposited on the surface of 
still water, and they vary in number with the species: Anopheles and 
Stegomyia deposit 40 to 50 ova, singly or in small groups, each ovum 
resting on its side; Culex deposits 300 to 400 ova, in large, coherent 
masses, the individual ova being on end. The ova are very resistant, 
and may mature even after several months of drying. In from twelve 
hours to three or four days, depending upon the temperature of the water 
and the air, the ova develop to larvae— minute, whitish or brownish, 
worm-like bodies that hang below the surface of the water and exhibit 
an active wiggling motion, whereby (about once a minute) they come to 
the surface to breathe, through a respiratory tube that projects from the 
last abdominal segment. The larvae may remain capable of maturation 
after several months of unfavorable environmental conditions, even 
freezing in ice. After existing in the larval stage for about one week 
(Culex and Stegomyia) to two weeks (Anopheles), during which time 
several moultings occur, the pupae appear — distinguishable from larvae 
chiefly by the greater size of the thoracic segment, but also by their dis- 
position to float on the water (being lighter than water). At the end of 
from two days (Culex and Stegomyia) to five days (Anopheles), the imago 
or adult insect emerges from the pupal shell. The first deposition of 
eggs occurs about twenty days later, and recurs at intervals of several 
days — each female mosquito being said to give rise to at least twelve 
generations in a season. The Anopheles mosquito becomes infected 
with the malarial parasite by sucking the blood of a malarious subject. 

Plasmodium Malarle in Man. — Craig distinguished four distinct 
species: Plasmodium vivax (Grassi and Feletti), the tertian parasite; 
Plasmodium malariae (Marchiafava and Celli), the quartan parasite; 
Plasmodium falciparum (Blanchard), the tertian estivo-autumnal para- 
site; and Plasmodium falciparum quotidianum (Craig), the quotidian 
estivo-autumnal parasite. Each species passes through two different 
cycles of development, the one in man, the other in the mosquito. 

The Tertian Parasite. — The tertian parasite is seen in its earliest 
stage within the infected erythrocyte as a small (2/x in diameter), round- 
ish, hyaline, unpigmented, and actively amoeboid body — protruding 
and retracting pseudopodia. This increases in size and soon accumulates 
a number of fine, reddish-brown pigment granules which it has elaborated 
from the hemoglobin of the infected erythrocyte, and which, reflecting the 
amoeboid movement of the parasite, appear actively motile. When 
almost or quite full grown the parasite is roundish, distinctly outlined, 
actively amoeboid, and contains motile pigment granules which are 
usually distributed rather diffusely (sometimes in small clumps) through- 



200 PROTOZOAN INFECTIONS 

out the parasite; what are usually described as a nucleus and a nucleolus 
may be distinguished in stained specimens. The containing erythrocyte 
is much swollen and pale. At the end of thirty-six hours, as maturity is 
reached, scarcely any of the distended erythrocyte (which may be almost 
twice the normal size) is visible, the amoeboid motion has lessened, and 
the pigment granules, much increased in number, tend to collect in the 
centre of the parasite. Soon radial striations appear and divide the 
parasite into from twelve to twenty-four (an average of sixteen) segments, 
which contain no pigment and are arranged usually in two rows, one 
toward the periphery and the other toward the centre, though they may 
be arranged irregularly. Toward the end of forty-eight hours the ery- 
throcyte has been entirely destroyed, and segmentation of many of the 
parasites (sporocytes) occurs; the free segments, liberated in the blood 
stream, float about as unpigmented bodies, and soon re-infect other 
erythrocytes and again pass through this so-called asexual cycle of de- 
velopment. Some parasites, however, do not undergo segmentation, 
but persist as large parasites with actively motile pigment granules — the 
sexually differentiated microorganisms (gametocytes) designed for the 
sexual cycle of development in the mosquito. Remnants of the mother 
parasites, consisting mainly of inanimate bodies and pigment, are ab- 
sorbed by the leukocytes and the vascular endothelium, and thus removed 
from the circulation. The malarial paroxysms (chill and fever) occur at 
the time of segmentation (liberation of toxins) — thus at intervals of 
forty-eight hours (every third day). In some cases a double tertian 
infection occurs, and segmentation of the different sets of parasites occur- 
ring on alternate days, a malarial paroxysm occurs every day (quotidian 
malarial fever). 

The Quartan Parasite. — In general the quartan parasite resembles 
the tertian, but it presents certain noteworthy differences. In its 
early stages the quartan parasite is smaller than the tertian and has a 
more definite contour; its amoeboid movements are more sluggish; the 
pigment granules are coarse, rod-like in shape, and deep brown or 
blackish in color; and the containing erythrocyte does not increase in 
size, but remains normal, or perhaps decreases in size, and becomes 
darker, yellowish, yellowish green, or brassy in color. As the parasite 
increases in size, the amoeboid movement gradually ceases, so that when 
full-grown (toward the end of seventy-two hours), the parasite is entirely 
motionless, distinctly outlined, and completely fills the containing 
erythrocyte. Throughout most of its life cycle the pigment granules are 
distributed around the periphery of the parasite, but toward the end of 
seventy-two hours these tend to collect in the centre to form a star- 
shaped mass radiating from the centre. Segmentation occurs as in the 
tertian organism, but the segments are more distinctly outlined than in 
the tertian parasite, they are fewer in number (six to twelve), and they are 
arranged regularly around the pigment (so-called daisy or marguerite 
forms). Like the tertian organism, some of the quartan parasites do not 
undergo segmentation, but persist to undergo the mosquito phase of 



MALARIAL INFECTIONS 201 

development. The malarial paroxysms (chill and fever) occur concur- 
rently with segmentation — about every seventy-two hours (every fourth 
day). Double or even triple infections with the quartan parasite may 
occur, giving rise to a malarial paroxysm on each of two succeeding days 
with a free day, or to a daily paroxysm. 

The Estivo-autumnal Parasite. — Two types of the estivo-autumnal 
parasite may be distinguished, the quotidian and the tertian. The 
quotidian estivo-autumnal parasite is seen in its earliest stages in the in- 
fected erythrocyte as a small, round, hyaline or ring-shaped body 
(signet ring), with indistinct outlines, and markedly amoeboid (rapid but 
not wide movements). The containing erythrocyte is usually smaller 
than normally, greenish or brassy in color, and sometimes contains two 
or even three parasites. Some of the parasites become pigmented, in 
some cases apparently only those in the organs (the spleen and the bone 
marrow), those in the circulating blood remaining unpigmented; the 
pigment at first consists of fine, dust-like particles, slightly motile and 
arranged usually about the periphery; as the parasite grows the pigment 
tends to collect in the centre and then becomes motionless. When full 
grown the parasite is scarcely more than one-fourth or one-third the 
size of a normal erythrocyte (distinction from the ordinary tertian and 
quartan parasite). Segmentation occurs (in the organs rather than in 
the circulating blood) at the end of twenty-four hours, and often quite 
obviously within the erythrocyte; six to eight spores are formed. The 
tertian (so-called malignant) estivo-autumnal parasite differs from the 
quotidian parasite in that the ring form is larger, more irregular in 
outline, more sharply defined, and more refractile; it requires forty- 
eight hours to complete its cycle of development; the pigmented stage 
lasts twenty-four hours or more, and during this time the parasite is 
actively amoeboid and the pigment exhibits a characteristic oscillatory 
movement not seen in the quotidian parasite; and when full grown the 
parasite fills one-half or two- thirds of the infected erythrocyte. This 
parasite differs from the ordinary tertian organism in being smaller 
(at corresponding stages of development); in sometimes assuming ring 
forms and giving rise to crescents; in the more scanty and less active 
pigment; in occasioning shrinkage (rather than swelling) of the infected 
erythrocyte; and in giving rise to a less number of spores (eight to fifteen). 
Segmentation occurs in the internal organs, and often intermittently — 
whence the irregularity of the clinical manifestations. In both varieties 
of estivo-autumnal infection, at the end of about a week, other character- 
istic parasites (with coarse, centrally situated, pigment granules) appear 
in the blood— crescent-shaped, spindle-shaped (cigar-shaped) , and sphe- 
roid (or ovoid) bodies. These do not sporulate, but represent sexually 
differentiated forms (gametocytes) designed for the life cycle of the 
parasite in the mosquito. The quotidian, as contrasted with the tertian, 
crescent is smaller, shorter, and plumper; its extremities are rounded 
(never pointed); its protoplasm is less granular; and its pigment is less 
in amount. The estivo-autumnal parasites give rise to the more severe 



202 PROTOZOAN INFECTIONS 

malarial infections, to many latent or masked infections, and to the so- 
called pernicious or malignant infections, especially common in tropical 
and subtropical regions; but the ordinary tertian or quartan infections 
may become pernicious. 

Plasmodium Malarle in the Mosquito. — When a mosquito of 
the genus Anopheles bites a malarious subject, it sucks into its stomach 
blood containing the sexually differentiated forms of the malarial parasite 
(gametocytes) — large spheroidal non-sporulating forms in the tertian 
and the quartan infections, and crescents and spheroid (or ovoid) forms 
in estivo-autumnal infections. These develop into flagellating and non- 
flagellating spheres, the former representing male elements (micro- 
gametocytes) and the latter female elements (macrogametocytes). 
The flagella (microgametes) are cast off by the male elements, and pene- 
trating fertilize the female body (macrogamete). The impregnated 
female parasite now penetrates the wall of the midgut of the mosquito 
and continues its development in the muscular coat, in which, at the end 
of two days, minute, refractile, and pigmented spheres may be found. 
These rapidly increase in size and become encapsulated. At the end 
of a week they may have attained a diameter of 70//, and they contain 
a large number of delicate spindle-shaped filaments, about 14/z in length 
(sporozoites). The mother cell (zygote) soon ruptures, setting free 
an enormous number of sporozoites, which speedily accumulate in the 
salivary glands of the mosquito, and are inoculated into man through 
the proboscis of the mosquito when next it bites. The sporozoites soon 
develop into young hyaline forms, and, invading the erythrocytes, pass 
through the asexual cycle of development and give rise to the clinical 
manifestations of malaria. Fertilization of the macrogamete may also 
be studied on the warmed stage under the microscope, as was originally 
observed by W. G. MacCallum. 

Pathology. — The most striking lesions in the acute infections consist 
of destruction of the erythrocytes and certain resultant changes. The 
blood as a whole is hydremic, the erythrocytes are decreased in number 
(due to direct destruction and probably also in consequence of a toxin 
produced by the parasites); the color index is reduced, and granular 
degeneration and polychromatophilia occur; the mononuclear leukocytes 
are increased; many of the polynuclear leukocytes are much pigmented; 
and free pigment is found in the plasma. The spleen is enlarged; the 
capsule is tense and may rupture; many infected erythrocytes are found 
in the pulp; and considerable pigment is free and enclosed within macro- 
phages. The liver is enlarged, and hyperemic, and may reveal foci of 
necrosis due usually to capillary thromboses; the capillaries may contain 
many parasites. The kidneys are often swollen and may show some 
cloudy swelling, and may reveal pigmented leukocytes and parasites, 
acute nephritis is not uncommon in estivo-autumnal infections. The 
bone marrow often contains many segmenting parasites. In pernicious 
infections hemoglobinemia and parenchymatous hemorrhages are com- 
mon, and the capillaries throughout the body (brain, gastro-intestinal 






MALARIAL INFECTIONS 



203 



tract, kidneys, etc.) may be found packed with parasites. In chronic 
malaria there is usually a high-grade anemia ; great enlargement, indura- 
tion, and pigmentation of the spleen (ague cake) ; enlargement, pigmenta- 
tion of the endothelial and Kupffer's perivascular cells, and occasion- 
ally cirrhosis of the liver; enlargement and pigmentation of the kidneys; 
pigmentation of the gastro-intestinal mucous membrane, especially of 
the solitary glands and Peyer's patches; and in the bone marrow replace- 
ment of the fat by proliferated marrow cells, new bloodvessels, and pig- 
mentation. 

Symptomatology. — The following clinical types of the malarial infec- 
tions may be distinguished : (1) Tertian infection ; (2) quartan infection ; 
(3) estivo-autumnal infections; and (4) chronic malarial cachexia. 
The tertian and the quartan infections comprise the regularly intermittent 
fever of the older writers, and the estivo-autumnal infections the irregular, 
remittent, continued, and pernicious fevers. 



Fig. 4 



DAY OF 
MONTH 


10 


11 


12 


13 


14 


15 


TIME OF 
DAY 


n 


2 


s L 


= 


2 


2 
< 


= 


= 


2 


2 


= 


= 


6 

2 


s 


= 




■ 


i 


I 


s 


2 


s 


= 


= 


2 


2 


? 


= 


D 

2 


2 


- - N 


2 




d 

'" 2 


2 


:; 


2 


_105° 
J 104° 
2 103° 
-102° 
? 101° 
E 100° 
1 99° 
H 98° 


3ip 










J 


= 




= 




| 




| 


1 


1 




z 


1 


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- 


| 


1 






l 




§ 




| 


| 


_5lp 


1 


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- 



The temperature in tertian malarial infection (Craig). 



Tertian Infection. — Tertian malarial infection is characterized 
by a so-called malarial paroxysm, consisting of chill, fever, and sweat, 
recurring at intervals of forty-eight hours (every third day), corresponding 
with the life cycle of the tertian parasite (Fig. 4). The period of incuba- 
tion is not definitely known; it is said to vary from thirty-six hours (experi- 
mentally) to twenty days. Prodromal symptoms, consisting of malaise, 
headache, restlessness, yawning, stretching, loss of appetite, etc., usually 
precede for several days the definite malarial paroxysm. The initial 
manifestation of the paroxysm, the chill, is, as a rule, sudden in onset, and 
it is usually severe, the entire body being more or less violently agitated. 
The skin is pale, cold, cyanosed, and presents the peculiar appearance 
described as goose-flesh (cutis anserind). The patient complains bitterly 
of the violent agitation and cold, and seeks to mitigate his distress by 
additional bedclothes, and hot water bottles. His discomfort is sometimes 
increased by nausea and vomiting and intense headache (congestion 
of the cerebral vessels). The pulse is frequent, and often hard and 



204 PROTOZOAN INFECTIONS 

irregular; and the urine may be increased in amount. The chilling of 
the body is superficial only, since with the advent of the chill (if not pre- 
viously) the temperature begins to rise, and at the height of the chill the 
rectal (or the axillary) temperature may be 103° to 106° F. or more. This 
so-called cold stage lasts for from fifteen minutes to an hour, and is 
succeeded by the hot stage. The patient begins to complain of alternat- 
ing sensations of heat and cold, until gradually the subjective sensation 
of cold disappears and the surface of the body becomes intensely hot, 
whereupon he complains as much of the heat as he did of the cold. 
The face is flushed, the conjunctiva? injected, the general integument 
congested; the pulse becomes full, bounding, and perhaps dicrotic; 
the respirations are quickened; throbbing headache and thirst are often 
marked; and in severe infections stupor and delirium may supervene. 
Cutaneous eruptions — erythema, urticaria, and herpes — often develop, 
labial herpes being quite as common as in pneumonia. During this 
stage the temperature reaches its highest point — 105° to 106° F. or more, 
though occasionally it may be only 104° F. The hot stage lasts for from 
one to three or four hours or more, and ends abruptly with a sudden 
fall of the temperature to normal (intermittent fever) and a profuse 
sweat. The perspiration usually begins on the forehead and face and 
soon involves the entire body, and has been said to have a characteristic 
sperm-like odor; the pulse becomes slower and weaker; the headache 
and other subjective complaints cease; considerable urine may be 
voided; and the patient often falls into a sleep from which he awakens 
several hours later much refreshed, though often somewhat exhausted. 
The sweating stage lasts usually from one to three hours. 

The average duration of the tertian malarial paroxysm is from ten 
to twelve hours; it may be less when mild, and it is sometimes very severe 
and much prolonged. One, two, or all three stages may be much 
shortened or abortive. Frequently, especially in primary attacks and 
in children, there is not a distinct chill, but only chilliness, or merely 
pallor and cyanosis in children; or the hot stage alone may be present, 
the sweating being slight; or the fever may escape observation — where- 
upon the infection is likely to go unrecognized. 

During the paroxysm the spleen becomes enlarged and palpable, and 
may remain so. The skin may present a peculiar lemon-yellow tint — due 
to a rapidly developed anemia, a form of hemolytic jaundice, or abnor- 
mal deposition of pigment. A dry bronchitis, diarrhoea and other 
intestinal symptoms, etc., are not uncommon concomitant symptoms, 
and suggest special localizations of the toxic process. 

In some cases the paroxysms occur not every other day, but daily 
(quotidian intermittent fever): cases of double tertian infection in 
which the two sets of parasites mature on alternate days. After persist- 
ing for several weeks, the malarial paroxysms frequently tend to cease 
spontaneously, but in this event recurrence is very likely. When 
neglected the infection may become chronic (malarial cachexia), or 
rarely pernicious. 



MALARIAL INFECTIONS 



205 



Quartan Infection. — Quartan malarial infection is characterized 
by malarial paroxysms (chill, fever, and sweat) recurring at intervals of 
seventy-two hours (every fourth day) — corresponding with the life cycle 
of the quartan parasite (Fig. 5). In the event of a double quartan infec- 
tion a paroxysm occurs on each of two successive days and is followed 
by a free day; in the event of a triple infection a paroxysm occurs daily 
(quotidian fever). As a rule, the paroxysms in quartan infection, as 
contrasted with tertian infection, are more severe, though they are shorter 
(usually less than ten hours); nervous symptoms, such as headache, 
restlessness, etc, are more pronounced; delirium is more likely to occur; 
and the tendency toward perniciousness is somewhat more marked. 
Otherwise there is but little difference in the clinical manifestations of 
the two forms of infection. 



Fig. 5 



0AY OF 

MONTH 


14 


15 


16 


17 


18 


19 


20 


21 


TiME OF 
DAY 


V'-'Hrrl 


i zz ii'- z I 


v---ii----\ 


tli^ii = S 


i^iirrl 


i-- L -*i-- 


r s 


sLUs'sU-iS 


.LjJj*, 


105° 

T 104° 


==i : = 


~ ■ ^ 


~~^ 


jE 


■ = 


— '■ 




Ezjssi 


mmi 


% 103° 
£> 102° 


m 


Hpi 


- 


- — 1 = 


EEpq— 


- = 







Qp== 


IHHl 


g 101° 


—F 


V 


■= 


~ : = 


^h=p^ 


. '= 






=£~j=^ = 


H 100° 
£ 99° 


IB 


=p 


zzzl 


= 


=^=^1^ 


—~ = 






izj— yj=^^ 


£ no° 


; 


-— - : --=}= 


A '— -^A :=s=-—^ 


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=h ' \= 


-^H 




= 


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K 97° 






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— r- ~ =^=2^=7=^ 


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smi 




— — 




. = 


' 


■ = 


-^H* 


=^=^^ — ^ 


^^^= 



The temperature in quartan malarial infection. (Craig.) 

Estivo-autumnal Infections. — These are most common in tropical 
and subtropical regions, where they prevail throughout the year, but they 
are also rather prevalent in the temperate zones, especially during July, 
August, September, and October (whence the name). As a rule, they are 
more severe than the ordinary tertian and quartan infections, and they 
are more likely to become pernicious. The following varieties may be 
differentiated: (1) Tertian estivo-autumnal infection (the most com- 
mon); (2) quotidian estivo-autumnal infection; (3) pernicious estivo- 
autumnal infection, of which the comatose, the algid, and the hemor- 
rhagic forms are the most common. 

Tertian Estivo-autumnal Infection. — The prodromal symptoms, as 
a rule, are similar to those of the ordinary tertian and quartan infections. 
The cold stage does not last more than a half hour, and there is usually 
chilliness rather than a distinct chill; but the patient complains of head- 
ache, pain in the back and legs, nausea, and perhaps vomiting; he is 
much depressed mentally, and he may be slightly stuporous or even 
delirious; the skin and mucous membranes are cyanosed; the pulse is 
frequent, weak, and irregular; the respirations are rapid and shallow; 



206 



PROTOZOAN INFECTIONS 



and the internal temperature is elevated (Fig. 6). At the onset of the hot 
stage, the temperature has reached 103° to 104° F. ; whereupon it oscillates 
slightly for several hours, then falls a degree or two or three (pseudo- 
crisis), rises again, perhaps higher than it was previously (precritical 
rise), and finally falls rapidly to normal or below (true crisis). The entire 
fever period is much longer than in ordinary tertian infections, and may 
last twenty, thirty, or even forty hours. Concurrently with the crisis 
the patient sweats, but the sweating is usually much less marked than in 
ordinary tertian infections. In many cases the paroxysms recur regularly 
every forty-eight hours, corresponding with the life cycle of the parasite — 
a fact not sufficiently recognized; but in many cases the manifestations 
are quite irregular. The temperature may rise slowly or fall by lysis; 
and it frequently becomes remittent or continuous in consequence of 
anticipation (overlapping) or retardation of the paroxysms (especially 



Fig. 



DAY OF 
MONTH 


23 


24 


25 


26 


27 


28 


29 


30 


TIME OF 
DAY 


d 


m L 


^ 


s 


^ 


ot 


£ E - \- 


2 


si 


Ol 


S 


£_ 


- 5 


< 


1 • 

- - s 


E 


ielo> 


6 


£ L 

< " 


ra 


12 M. 
3 P.M. 
6 " 
9 " 
12 MID. 


3 A.M. 

12 M. 
? P.M. 

12 MID. 


|;li 


A\~ - 


2 


E 


IS 


o- 


2 


i 


ID 


_ 105° 
£ 104° 
2 103° 
i 102° 
? 101° 
£ 100° 
£ 99° 
" 98° 


| 




| 


1 
















jj 










|g 










j I ItjoM j 


^ff 


oj— j— 














1 

111 
< 



The temperature in tertian estivo-autumnal malarial infection. (Craig.) 

common in estivo-autumnal infections), reduplications of the paroxysms 
due to double or mixed infections, etc. ; and sometimes there is a moderate 
degree of fever between irregularly recurring paroxysms attended by 
more marked fever. In consequence, the infection has been and fre- 
quently is mistaken for typhoid fever: a coated tongue, enlarged spleen, 
bronchitis, tympanites, and diarrhoea alternating with constipation, 
increase the diagnostic difficulties — whence the ill-advised term, typho- 
malarial fever. The patient is depressed, even prostrated, and complains 
of divers subjective complaints, not only during the paroxysms, but also 
between them. Frequently the fever subsides at the end of a week or 
ten days, but it may continue much longer. In severe infections, loss "of 
appetite, nausea, bilious vomiting, and jaundice, suggest the designations 
bilious remittent fever, gastrobilious fever, jungle fever, etc. These 
often assume pernicious tendencies. 

Quotidian estivo-autumnal infection frequently cannot be differenti- 
ated clinically from the tertian estivo-autumnal infection, but, as a rule, 
it is characterized by more severe chilly sensations or distinct chills 
and more marked sweating (though neither is as marked as in the ordinary 



MALARIAL INFECTIONS 



207 



tertian and quartan infections); the paroxysms recur daily, the fever 
rising rapidly to 103° or 104° F., and falling suddenly within six or eight 
hours to normal (Fig. 7) ; but the paroxysms frequently become prolonged 
to twelve, sixteen, or twenty-four hours (due to irregular generation of 
parasites) — whence a remittent or continued fever results (especially in 
pernicious cases). Postponement of the paroxysms occurs in cases 
tending to spontaneous recovery. 



Fig. 7 



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The temperature in quotidian estivo-autumnal malarial infection. (Craig.) 



Pernicious Estivo-autumnal Infections. — Depending upon the special 
prominence of certain symptoms, many varieties of pernicious estivo- 
autumnal infections have been described, such as comatose, delirious, 
convulsive, syncopal, paralytic, algid, gastro-intestinal, bilious, choleraic, 
dysenteric, cardialgic, hemorrhagic, hemoglobinuric, pneumonic, etc.; 
but these represent variations in degree, rather than differences in kind. 
The so-called comatose, the algid, and the hemorrhagic forms are the 
most common and merit special mention. 

The comatose (the most common) form is due usually to the tertian 
estivo-autumnal parasite, and is characterized by symptoms of intense 
cerebral congestion (intimately associated with thrombi of parasites in 
the cerebral capillaries and necrotic and other changes about them). 
At the onset there is often a chill and fever, as in other malarial infections, 
though nervousness and mental depression (rarely slight delirium) may be 
early obtrusive features. Soon the patient becomes stuporous and then 
comatose. The coma may come on with the first paroxysm, or not until 
the second or third (or later), and although it may be preceded by mental 
disturbance, it may develop suddenly, persist, and lead to death within 
several hours or two or three days. On the other hand, the coma 
may intermit, that is, develop with the rise of the temperature and clear 
up when the fever falls — in which event it rarely lasts more than twelve 
to twenty-four hours; but a second or third attack may prove fatal. 
The fever is high, but it may be as low as 101° F.; the face is flushed, or 



208 PROTOZOAN INFECTIONS 

subicteric or leaden, if anemia is present; the pulse is slow and full at 
first, but it soon becomes weak and irregular; the spleen is enlarged; the 
pupils may be equally contracted, or unequally contracted or dilated; 
muscular twitchings are common; and the sphincters may become 
paralyzed. 

The algid form (congestive chills) is characterized by nausea, vomit- 
ing, and purging, leading to collapse and simulating the algid stage of 
cholera. Usually there is no chill, but chilliness is complained of; the 
internal temperature may become considerably or moderately elevated, 
but it is not infrequently subnormal; the pulse is rapid, weak, and ir- 
regular; the general integument and the visible mucous membranes are 
pale and livid, and the skin is covered with a profuse clammy sweat; 
the eyes are sunken, the pupils dilated, and the Hippocratic facies de- 
velops. The urine is often lessened in amount or suppressed, and jaun- 
dice and grave nervous symptoms may supervene (simulating yellow 
fever). The patient may die within a few hours, or at the end of 
several days, from profound asthenia. 

The hemorrhagic form is characterized by bleeding from the mucous 
membranes of the body (mouth, stomach, intestine, rectum, vagina, 
etc.), or into the skin and the interstices of the body; but special interest 
attaches to a peculiar hemorrhagic form of the infection known as 
blackwater fever, hemoglobinuric fever, or malarial hemoglobinuria. This 
is rather common in our own Southern States, and in Central America, 
Italy, and Africa. It usually follows estivo-autumnal infections, but 
it has been observed after ordinary tertian and quartan infections. 
Apparently it occurs only in persons who have had repeated attacks of 
malaria and have become anemic or cachectic. The parasites, as a rule, 
are present in the blood before the onset of the attack, but during the 
attack they are often absent. The immediate cause of the attack is not 
known: those who have seen the disorder are not agreed as to whether 
or not quinine is of significance in provoking the attack; but there is 
some evidence that quinine is of etiological importance in some cases, 
and it often appears to be harmful if administered during the attack 
when the parasites are absent from the blood (said to be referable to a 
hemolytic action of the quinine on the erythrocytes). In some cases 
the patient gives a history of a few days of intermittent or remittent 
fever with increasing biliousness, then a sudden chill and bloody urine; 
in other cases, especially those that develop late in the fall or winter, there 
may have been for some time irregular outbreaks of malaria, then the 
prodromal symptoms of another attack followed by the bloody urine 
(said by some observers to be provoked by the quinine taken to ward 
off the impending paroxysm). The urine contains methemoglobin, 
hemoglobin, hematin, degenerated erythrocytes, leukocytes, biliary 
coloring matter, tube casts, and considerable albumin. In favorable 
cases the urine becomes clear in from three or four hours to three or 
four days; but the other malarial manifestations may continue. In 
other cases the hemoglobinuria recurs periodically. Death may occur 



MALARIAL INFECTIONS 209 

on the first day from marked toxemia and coma, or it may occur later 
from the effects of the blood destruction, suppression of the urine and 
uremia, and general exhaustion. 

Chronic Malarial Cachexia. — This is a condition of pronounced 
anemia with enlarged spleen that develops in those the subjects of long- 
continued malarial infection. The symptoms are those common to 
high grade anemia — asthenia, breathlessness, palpitation of the heart, 
and slight oedema about the ankles. In addition there is a subicteric hue 
to the skin or a yellowish-brown pigmentation; the spleen is enlarged; 
hemorrhages may occur into the retina and elsewhere (especially the 
gastro-intestinal tract) ; and the patient is subject to irregular attacks of 
fever of variable duration with intervening periods of apyrexia. 

Latent and Masked Malarial Infections, — These are by no 
means uncommon, and though usually due to the estivo-autumnal para- 
site, they may be due to the ordinary tertian or quartan parasite. These 
infections, though they often manifest a noteworthy periodicity, simulate 
a wide variety of disorders, such as neuralgia (supra-orbital, occipital, 
intercostal, sciatica, etc.), paresthesias, anesthesias, paralyses, hemi- 
plegia, ataxia, amaurosis, deafness, etc., and certain gastro-intestinal 
disorders, such as gastro-enteritis, dysentery, etc. In many of the 
cases the parasite may be found in the blood; in other cases, the symp- 
toms subside promptly upon the administration of quinine. Tubercu- 
losis, dysentery, cardiac degeneration, cirrhosis of the liver, nephritis, 
orchitis, parotitis, gangrene of the skin, etc., have been observed as com- 
plications or sequels of malarial infections. 

Diagnosis. — The ordinary tertian and quartan infections are usually 
recognizable from the clinical manifestations, but the diagnosis is easily 
rendered certain by a microscopic examination of the blood. This 
should not be neglected in any case in the diagnosis of which malaria 
enters as a possibility. In the event of more continued fever, it may be 
necessary to exclude typhoid fever, tuberculosis, pyogenic infections 
(especially acute ulcerative endocarditis), etc. Typhoid fever may be 
excluded by the absence of the Gruber-Widal reaction, the presence of 
malarial parasites in the blood, and the response of the symptoms 
to quinine; in fact, that fever that does not respond to quinine within 
four or five days may be said not to be malaria. Tuberculosis may 
be excluded by the history of the patient, the associated general symp- 
toms, the physical signs, the presence of tubercle bacilli in the sputum or 
cerebrospinal fluid (or choroid tubercles), and the absence of malarial 
parasites in the blood, and the non-response of the symptoms to quinine. 
Most of the pyogenic infections, of which ulcerative endocarditis is a 
type, are attended by leukocytosis (which is absent in malaria), they do 
not respond to quinine, and malarial parasites are not found in the blood. 

Prognosis. — In the ordinary tertian and quartan infections the prog- 
nosis is good; the disorders are quite amenable to treatment. The 
prognosis is also relatively good in many of the latent and masked 
infections, though they may last a long time. But the outlook is very bad 
14 



210 PROTOZOAN INFECTIONS 

in many of the estivo-autumnal, especially the pernicious, infections — 
the mortality being very high. 

Treatment. — Prophylaxis. — The malarial infections may be prevented 
by protecting all persons from the bites of mosquitoes. In malarious 
districts the windows and doors of all houses should be screened, and 
additional protection should be afforded by surrounding the beds with 
mosquito netting, especially the beds of malarious subjects (to prevent 
infection of uninfected mosquitoes). Furthermore, the breeding places 
of mosquitoes should be destroyed by filling up and draining swamps, 
and preventing stagnation of surface water. Larvae should be de- 
stroyed by coating the surface of all stagnant pools with kerosene (one 
ounce to each fifteen square feet of water) — whereby the larvae are de- 
prived of oxygen; this should be repeated every three or four weeks. 
Small fish also are of service in destroying the larvse. Oil of pennyroyal 
or of eucalyptus (which is obnoxious to mosquitoes) may be smeared 
on the hands by those obliged to work out of doors in malarious districts. 
Five to ten grains (0.3 to 0.6 gram) of quinine, once or twice a week, is 
also of service in warding off malarial attacks. 

Quinine is a specific remedy and the only drug that really can be 
depended upon. Following ancient custom, it is wise to deplete the liver 
and to unload the bowels by a preliminary dose of calomel (10 grains, 
0.6 gram), followed by a saline. Since the quinine is most efficacious 
when the parasites are free in the blood plasma, rather than when they 
are within the erythrocytes, it is desirable to have an adequate amount 
of quinine in the circulation at the time of sporulation. Therefore, 
four to six hours before the expected paroxysms in tertian and quartan 
infections, 15 to 30 grains (1 to 2 grams) of quinine bisulphate or 
bihydrochlorate should be given in solution (or in capsule or cachet, but 
not in pill form, since the pills often do not dissolve). If administered 
only shortly before the paroxysm the quinine will not prevent it, but 
will exert a deleterious effect on the parasites and prevent a recurrence. 
After the initial dose, it is wise to continue the quinine in from 10 to 20 
grain (0.6 to 1.3 gram) doses for several days, and then in 5 grain (0.3 
gram) doses daily for a week, and thereafter at intervals of a week for 
a month. In estivo-autumnal infections, similar doses, as a rule, are 
effectual, but in severe infections larger doses (up to 60 grains, 4 grams, 
or more, daily) may be required. In pernicious types of the infection 
it is often necessary to bring the system rapidly under the effects of the 
quinine, in which event it should be administered hypodermicly or 
intravenously: 15 to 30 grains (1 to 2 grams) of the bihydrochlorate, or 
of the hydrochlorate of quinine and urea, in 2 drams (30 c.c.) or more 
of physiological saline solution; if necessary, this may be repeated every 
two to four hours. During the attack of blackwater fever, quinine should 
not be administered, but it may be given in the intervals if parasites are 
found in the blood. No really efficient substitute for quinine has been 
discovered; methylene blue is a poor substitute, but may be given in 
doses of 1 to 4 grains (0.06 to 0.25 gram) when quinine cannot be taken. 



DISTOMATOSIS 211 

During the malarial paroxysms the patient should be made as com- 
fortable as possible — hot water bags during the cold stage, and tepid 
sponging and cooling drinks during the hot stage. Unduly severe parox- 
ysms should be controlled by an opiate. If necessary, the circulation 
should be supported by stimulants — strychnine and alcohol. Vomiting 
may be controlled by counterirritation to the epigastrium, cracked ice, 
sips of hot water, spirit of chloroform, a small amount of dry champagne, 
cerium oxalate and bismuth, etc. 

Many latent and masked infections are immediately relieved by one 
or two large doses of quinine; others require the prolonged use of the 
drug. Warburg's tincture is sometimes efficacious. In chronic malarial 
cachexia, removal to a non-malarious region, preferably at a high 
altitude, arsenic (Fowler's solution or arsenous acid), small doses of 
quinine and iron, or Warburg's tincture will be found efficacious. 



METAZOAN INFECTIONS. 



DISTOMATOSIS. 

(Distomiasis; Trematode Infections; Fluke Infections.) 

In man there are four important clinical forms of distomatosis — pul- 
monary, hepatic, intestinal, and venal or hemal distomatosis. 

Pulmonary Distomatosis (Lung-fluke Disease); Paragonimiasis; 
Parasitic Hemoptysis. — Pulmonary distomatosis occurs principally in 
Japan and China, but also in the United States, the Philippines, and 
Formosa. The parasite, Paragonimus (Distoma) westermanii, is an oval 
spinose fluke, somewhat pinkish in color, and measuring from 7.5 to 16 
mm. long, 4 to 8 mm. broad, and 2 to 5 mm. thick. The original host has 
not been determined with certainty, but the organism has been found in 
man, cats, dogs, swine, etc. The source of infection in man is not known, 
but it is probably contaminated food or water. The adult parasites are 
found in cysts in the lungs, pleura, brain, liver, abdominal cavity, etc. 
The symptoms consist of cough, yellowish, reddish, or rusty-brown 
sputum, in which ova (smooth, oval organisms, 80 to 100 p. in length, 
by 40 to 60 pt in breadth) may be found, often in great abundance (12,000 
daily). In some cases attacks of more or less severe hemoptysis occur. 
The liver, brain, eyelids, etc., may become involved, and death not 
infrequently results. 

Hepatic Distomatosis (Liver-fluke Disease.).— Six different species 
of flukes have been found in connection with hepatic distomatosis: (1) 
Opisthorchis sinensis (Distoma sinense), the most important, the cause 
of Asiatic opisthorchiasis or Japanese liver-fluke disease. The organism 
is an elongate, lanceolate, non-spinose trematode, 9.7 to 20 mm. long and 
2 to 5 mm. broad; it is of a reddish color and very transparent. Its chief 



212 



METAZOAN INFECTIONS 



anatomical characteristic is the branched condition of the testicles. 
The eggs are dark brown in color, have a well-defined operculum, and 
measure 24 to 30 by 15 to 17.5 ji. Man, cats, and dogs appear to be nor- 
mal hosts. Infection seems to be acquired from swallowing the free 
cercaria or indirectly from eating an infected water animal (snail, fish, etc.) 
or food contaminated by infected water. (2) Opisthorchis felineus, the 
cause of Siberian opisthorchiasis or Siberian liver-fluke disease. Cases 
in man have been reported in Siberia and Prussia. The organism is a 
lanceolate, non-spinous trematode, 8 to 18 mm. long and 1.25 to 2.5 mm. 
broad; the testicles are lobate, but not branched. The eggS are yellow- 
ish brown, oval, have a well-defined operculum, and one side flatter than 
the other, and measure 26 to 30 by 11 to 15 //. The cat, dog, fox, and 
glutton are natural hosts. Infection seems to be acquired from eating 
raw fish. (3) Opisthorchis noverca, the cause of Indian opisthorchiasis 
or Indian liver-fluke disease, which is very rare. (4) Dicroccelium 
lanceatum, the cause of dicrocceliasis (lancet-fluke infection). The 
organism is a lancet-shaped trematode, 4 to 9 mm. long and 2 to 4 mm. 
broad. The eggs are dark brown and thick shelled, have a distinct 
operculum, and measure 38 to 45 by 20 to 30 p.. Cattle and sheep are 
normal hosts. The infection is rare in man, and probably always 
accidental. (5) Fasciola hepatica, the cause of fascioliasis. The 
organism is a broad flattened, oval trematode, 18 to 30 mm. long and 
4 to 13 mm. broad. The eggs are yellowish or brownish in color, 130 
to 145 by 70 to 90 jjl, and they have a distinct operculum. Cattle, goats, 
and sheep are normal hosts; snails are the intermediate host. Infection 
is acquired by swallowing the encysted cercaria. The infection is rare 
in man. (6) Fasciola hepatica, or an organism allied thereto, is said to 
be the cause of a disease known as halzoun in Liban, Syria. These liver 
flukes enter the bile ducts and cause (mechanically and by irritation) 
stoppage of these passages. In early cases the liver is enlarged and 
hyperemic; in protracted cases it may be normal or lessened in size, and 
there may be some sclerosis. The symptoms consist principally of 
enlargement and tenderness of the liver, preceded, attended, or followed 
by diarrhoea (irregular and intermittent), with dark, sometimes bloody 
stools, occasionally slight fever (100°). Night blindness, intermittent 
ascites, anasarca, and epistaxis may occur. Anemia and emaciation 
supervene, and finally, after more or less improvement and relapses 
(diarrhoea, etc.), the patient usually dies. The ova are readily found in 
the stools. Preventive measures comprise destruction of infected animals 
and their excreta, the use in infected localities of boiled water and thor- 
oughly cooked food, and removal from infected regions. There is no 
efficient treatment. 

Intestinal Distomatosis (Intestinal Fluke Disease). — Intestinal 
distomatosis in man may be caused by: (1) Fasciolopsis buskii, the largest 
and most important; it measures 27 to 37 mm. in length, 5.5 to 14 mm. 
in breadth, and 1.5 to 2 mm. in thickness. It occurs especially in Asia, 
and is distinguishable from Fasciola hepatica by its large acetabulum 



DISTOMATOSIS 213 

and simple intestine. Infection is said to cause indigestion, nausea, 
headache, and diarrhoea with bloody stools. The ova which may be 
found in the stools measure 120 to 130 by 77 to 80 fi. Thymol and 
calomel are said to be capable of expelling the parasite. (2) Fasciolopsis 
rathonisi (reported once in Asia). (3) Heterophyes heterophyes, a 
minute harmless trematode found in the small intestine of man, dogs, 
and cats. (4) Gastrodiscus hominis (found in the cecum and colon of 
man in India). (5) Cladorchis (Watsonius) watsoni (reported once in a 
negro boy in Africa). 

Venal Distomatosis (Blood-fluke Disease, Bilharziosis; Egyptian 
Hematuria; Endemic Hematuria; Bilharzian Hematuria; Bilharzia 
Disease). — Blood-fluke infection in man may be due to: (1) Schistosoma 
haematobium (Bilharz), the African blood fluke, of which the male is 4 to 
15 mm. long and 1 mm. broad, and the female (carried in the gynecophoric 
canal of the male) longer and filiform. The eggs are 135 to 160 by 55 to 
66 ix, provided with a terminal spine, but no operculum. (2) Schistosoma 
japonicum (Katsurda), the Asiatic blood fluke, of which the male is 
7 to 12 mm. long, and 0.53 to 0.8 mm. broad; the female is 8 to 12 mm. 
long. The eggs are 60 to 90 by 30 to 50 /*, and are not provided with a 
terminal spine or an operculum. The source of infection is not definitely 
known, although there is increasing evidence that it occurs through the 
skin; drinking water cannot be eliminated; some observers believe that 
the urethra and the anus may be the infectious atria. The young 
worms live in the veins of the liver; the eggs are deposited in various 
organs (liver, intestine, bladder), and escape from the body with the urine 
and feces. One-half of the people of Egypt are believed to be infected; 
the males more than the females, and the rural rather than the urban 
population. The symptoms, (usually preceded by a period of incubation 
of four or five months) may be chiefly urogenital, consisting of irritability 
of the bladder, hematuria, pains in the lumbar region, left iliac fossa, 
thigh, or vulva, either spontaneous or on micturition; or they may be 
chiefly rectal, consisting of bloody stools, diarrhoea, and perhaps pro- 
lapse of the rectum. Secondarily cystitis, vesical calculus, urinary 
fistulas, nephritis, vaginal and rectal growths may develop. The patient 
becomes anemic and debilitated, and after a year or two may die, often 
from some intercurrent infection. The diagnosis is readily made by 
examining the urine and feces for the ova ; in some cases it may be neces- 
sary to examine scrapings from the bladder or the rectal wall to detect 
the parasites. The prognosis in mild infections is favorable, although 
relapses are common. The treatment is largely symptomatic and pallia- 
tive. Good results are said to follow the use of male fern (15 grains, 1 
gram, thrice daily), methylene blue (3 grains, 0.2 gram, thrice daily), 
santonin, quinine, etc. In rectal infections, local sedatives, as in dys- 
entery, often mitigate the suffering. 



214 



METAZOAN INFECTIONS 



TENIASIS. 

Infection; Hydatid Disease.) 



Teniasis may occur in one of two forms: (1) Intestinal infection with 
the adult cestode — tapeworm; and (2) somatic infection with the larval 
cestode. 

Intestinal Teniasis (Tapeworm Infection). — Stiles states that, so 
far as established, man seems to be the normal and sole host for the 
sexual stage of at least two large tapeworms, Taenia saginata and Taenia 
solium. Man, together with the dog, probably forms the normal host 
for a third large tapeworm, Dibothriocephalus latus. In common with 
rats and mice, man seems to have become a normal host for the dwarf 
tapeworm, Hymenolepis nana, although it has not been definitely 
established that the worm in man is exactly identical with that of the 
rodents. Occasionally, though rarely, as accidental host, man harbors 
the double-pored tapeworm, Digylidium caninum, of dogs and cats, 
the flavopunctate tapeworm, Hymenolepis diminuta, of rats, and the 
lanceolate tapeworm, Hymenolepis lanceolata, of ducks and geese. 
Other rarer examples of tapeworm infection in man have also been 
reported. 



Fig. 8 



Fig. 9 





Gravid segment of Taenia 
saginata, showing the lateral 
branches of the uterus, en- 
larged. (Stiles.) 



Gravid segment of Taenia solium, showing the lateral 
branches of the uterus, enlarged. (Stiles.) 



Taenia saginata (mediocanellata) the fat, unarmed, or beef (beef- 
measle) tapeworm, is the commonest tapeworm in North America. 
It may attain a length of 4 to 10 meters; the head, which may measure 



TENIASIS 



215 



2 mm. in breadth, is larger than that of Taenia solium, it is square-shaped, 
and has four large sucking disks, but no hooklets. There may be as 
many as a thousand segments ; only two ovaries are found in each mature 
segment; the uterus in the gravid segments has 15 to 35 slender dicho- 
tomous lateral branches each side of and shorter than the median stem 
(Fig. 8) ; genital pores lateral (marginal), irregularly alternate ; terminal 
segments attain a length of 16 to 25 mm., and a breadth of 4 to 7 mm.; 
the eggs are provided with a thick, dark, radially striated embryophore 
(so-called shell), and measure 30 to 40 by 20 to 30 /*. Cattle become 
infected by swallowing the embryo with food or water which has become 
contaminated by infected human feces. Man acquires the infection by 
eating beef, especially the tongue and the muscles of mastication, in- 
fected with Cysticercus bovis. 

Fig. 10 




Gravid segment of Dibothriocephalus latus, showing the rosette uterus in the median line. X 

(Leuckart.) 



Tcenia solium, the armed or pork-measly tapeworm, is most common in 
Europe and Asia. Usually it does not attain a length of more than 2 
to 3.5, sometimes 6 to 8 meters; the head is armed with a rostellum 
bearing a double row of hooks, of larger and smaller size, 22 to 32 in 
number; genital pores lateral (marginal) irregularly alternate; mature 
segments contain three ovaries, due to the fact that the ovary on the pore- 
side of the segment is divided; the segments may attain 10 to 12 mm. in 
length by 5 to 6 mm. in breadth; 800 to 900 segments may be present; 
in gravid segments, the median uterine stem possesses 7 to 15 lateral 
dichotomous branches on each side (Fig. 9); "eggs" (embryophore) are 
very similar to those of Taenia saginata, and measure 31 to 36 a in dia- 
meter. Hogs become infected by eating infected human feces; and man 
becomes infected by eating undercooked, underpickled, or undercured 
pork or wild boar meat, infected with Cysticercus cellulosae. 

Dibothriocephalus latus, the broad, or fish tapeworm, is cosmopolitan 
in its geographical distribution, but is most common in the vicinity of 
large bodies of water. It attains a length of 2 to 9 or 10 meters, and a 
maximum breadth of 20 mm.; it is usually grayish yellow to brownish 
in color, and composed of 3000 to 4200 segments, which are usually 
broader than long, especially in the anterior two-thirds of the strobila; 
the posterior segments become quadrate or even longer than broad, and 



216 METAZOAN INFECTIONS 

are especially characterized by the rosette spot (uterus) in the Centre 
(Fig. 10); the genital pores are ventromedial!; the eggs measure 68 to 
71 by 45 n, have a distinct operculum, and are laid during segmentation. 
Infection in man is acquired by eating raw or underdone fish, especially 
pike, ling or turbot, perch, and salmon, in the muscles and organs of 
which the larval stage of the parasite (a " plerocercoid") may be found. 

Hymenolepsis nana, the dwarf tapeworm, the smallest tapeworm 
known for man, is more or less cosmopolitan in its geographical distribu- 
tion; it is 5 to 45 mm. long and 0.5 to 0.9 mm. in maximum breadth, and 
is composed of 100 to 200 segments; the rostellum is armed; there are 
three testicles to each segment; the genital pores are unilateral; the eggs 
have two distinct membranes, the outer, 30 to 60 /x in diameter, and the 
inner, 16 to 34 p. in diameter, and present at each pole a more or less 
conspicuous mammillate projection provided with filamentous appen- 
dages. The source of infection in man is not definitely known, but there 
is reason to believe that it occurs from food infected by the excrement of 
rats and mice infected with Hymenolepsis nana fraterna (Stiles). Stiles 
believes that autoinfection is highly probable. 

Symptoms. — The symptoms of teniasis are quite variable, depending 
upon the species of tapeworm present, the number of parasites, and the 
age and general and nervous condition of the person infected. Often there 
are no symptoms, the parasite being an accidental finding in the stools. 
The appetite is variable; salivation may occur; nausea, vomiting, and a 
feeling of faintness may be present. Abdominal pains are common. 
They may be colicky or gastralgic in character, of varying intensity, and 
may be referred to different parts of the body. They may be intermittent, 
and may be increased by certain foods (herring, onions, and sour food), 
or decreased by a diet of milk, eggs, and oily food. Anemia is usually 
not marked in Taenia solium infection; it is more marked in Taenia sagi- 
nata infection, and still more marked in Dibothriocephalus latus infec- 
tion. Unequal pupils, disorders of vision, headache, tinnitus aurium, 
itching and dryness of the nose, epistaxis, and puruitus may be observed. 
Emaciation and loss of strength sometimes supervene in cases of long 
standing. 

Diagnosis. — The diagnosis is readily made from finding segments of 
the parasite in the stools, in the absence of which the disease at the most 
can be merely suspected. 

Treatment. — Prophylaxis is of the greatest importance; all meat at 
abattoirs should be carefully inspected, and that used for food should 
always be thoroughly cooked (which kills the parasites); infected stools 
also should be subject to incineration. With a view to cause expulsion 
of the tapeworm, the patient for a day or two should have the bowels 
thoroughly evacuated by means of saline cathartics; he should eat very 
little (mostly fluids), and from about six o'clock in the evening nothing- 
whatever, this with a view to uncover the parasite, permit ready access 
thereto by the vermifuge, and favor relinquishment of the hold of 
the parasite to the mucous membrane. In the morning one may give 



TENIASIS . 217 

1 to 2 drams (4 to 8 grams) of the oleoresin or the ethereal extract of male 
fern, and in about two hours a saline cathartic (not castor oil — which 
leads to absorption of the male fern and toxic symptoms) ; to an emulsion 
of the male fern one may add 2 minims (0.12 gram) of croton oil. Or 
one may use a decoction of pomegranate root: three ounces (100 grams) 
of the bark to 10 ounces (300 grams) of water, should be reduced to one 
half this amount by evaporation, and this taken in divided doses within 
two to three hours. The active principle pelletierine may be given in 
doses of 6 to 10 grains (0.4 to 0.6 gram); it also should be followed in an 
hour by a saline cathartic. Decorticated pumpkin seed, kooso, kamala, 
santonin, thymol, etc., have also been recommended. Often a large 
part of the worm is brought away, but the head remains; whereupon the 
worm continues to grow. Attempts to remove it should be made again 
at the end of a month or two, when segments again appear in the stools. 

Somatic Teniasis. — Infection with the larval stage of tapeworms 
may be due to: (1) Echinococcus granulosa (hydatid disease); (2) 
Cysticercus cellulosse, the larval Taenia solium; and (3) Sparganum 
mansoni and Sparganum proliferum. 

Echinococcus granulosa (Taenia echinococcus) is one of the smallest 
tapeworms; it is composed of a head with twenty-eight to fifty hooks, a 
short neck, and three or four segments; the first segment is immature, 
the second is mature, and the last is gravid and composes about one half 
of the total length (2.5 to 5 mm.) of the worm. The larval stage is the 
largest cestode known — the echinococcic hydatid; a subspecies is known 
as Echincoccus multilocularis. The gravid terminal segment of the 
tapeworm is discharged in the feces of the dog, and the egg gains access 
to the intermediate host (sheep, cattle, hogs, man, etc.) through con- 
taminated food or drinking water, or, in the case of man, possibly also 
from hands soiled while petting dogs. Upon arriving in the stomach, 
the oncosphere (six-hooked embryo) escapes from the shell and, by means 
of its hooks, bores its way to various parts of the body, especially to the 
liver. Here it comes to rest, and increasing gradually in size it presents 
a thick outer cuticle and an inner parenchymatic layer surrounding a 
cavity containing fluid. An outer connective tissue cyst is furnished by 
the host. Brood capsules arise from the parenchymatic layer and hang 
into the cavity; heads form in these brood capsules. Daughter and even 
granddaughter cysts may form and fall into the cavity of the mother 
cyst (so-called, endogenous echinococcus, common in man), or these 
daughter cysts may pass outside the mother cyst in the surrounding tissue 
(exogenous echinococcus, uncommon in man). Iceland is the home of 
the echinococcic infection, but it occurs in all parts of the world, although 
it is rather rare in this country. The infection is most common in the 
liver (56 per cent.), in the lung (8 per cent.), and in the kidneys (7 per 
cent.); but it may occur in any part of the body. 

Symptoms. — The symptoms consist of a slowly growing tumor, which 
may attain very large dimensions. The tumor may be more or less 
elastic, and may manifest on percussion a so-called hydatid thrill or 



218 METAZOAN INFECTIONS 

fremitus. The nature of the growth may be revealed by detecting 
hooklets in the fluid. Sugar in the fluid also is suggestive. A Wasser- 
mann and a precipitin-reaction test have been suggested. 

Treatment. — The treatment is surgical. 

Cysticercus cellulosoe, the larval form of Taenia solium, is an elliptical 
translucid, bladder-like structure, 6 to 12 mm. long by 5 to 10 mm. broad, 
with a white spot at its equator, due to the invaginated head. The 
disorder to which it gives rise, cysticercosis, is characterized by the 
presence of the parasite in the subcutaneous tissues, muscles, brain, 
spinal canal, eye, heart, lymph nodes, etc. It takes about three months 
for the parasite to develop from the six-hooked embryo (onchosphere) to 
the bladder worm stage, which may live in man as long as twenty years. 
The symptoms vary with the location and the number of parasites 
(sometimes several thousand). In slight infections there may be no 
symptoms; in severe infections, involving the brain there may be head- 
ache, visual disturbances (ophthalmoscopic examination may reveal 
the parasite), mental disorders, dizziness, paralyses, convulsions, etc. 
There is no effective medical treatment, although some good results 
with male fern have been reported. From accessible regions (the eye, 
for instance), the parasite may be removed surgically. 

Sparganum mansoni, a larval bothriocephalide tapeworm, has been 
rarely found in man (Japanese) in the peritoneal cavity, eye, urethra, etc. 
Sparganum proliferum has been reported once. 



NEMATHELMINTHIASIS 

(Roundworm Infection.) 

Uncinariasis (Ankylostomiasis; Hookworm Disease; Miner's 
Anemia; Egpytian Chlorosis). — Uncinariasis is common in tropical and 
subtropical countries. It is estimated that 90 per cent, of the rural popu- 
lation of Florida, and 30 to 80 per cent, of the miners of Germany are 
infected ; but the disorder occurs also in miners and others who are close 
in contact with the soil in more temperate zones. There are two para- 
sites: (1) Necator americanus (Uncinaria americana, Stiles), the New 
World hookworm, a cylindrical worm, 5 to 11 mm. long, and possessed 
of a dorsal and a ventral pair of lips at the mouth, a prominent dorso- 
median buccal tooth, and four buccal lancets; in the male, the dorsal 
ray of the bursa divides at the base and each branch possesses two tips ; 
in the female the vulva is the anterior half of the body; the eggs are thin- 
shelled, 64 to 72 fi long, by 36 to 40 a broad; they are oval with some- 
what bluntly rounded poles. (2) Ankylostoma duodenale (Uncinaria 
duodenalis, Dubini), the Old World hookworm, is 8 to 18 mm. in length 
and possesses in its mouth two pairs of strong, curved, ventral teeth, and 
one pair of knob-like dorsal teeth; the dorsomedian tooth of the 
buccal capsule is nil or practically so; a pair of ventral lancets is 
present in the buccal cavity; in the male, the dorsal ray of the bursa is 



NEMATHELMINTHIASIS 219 

divided two-thirds its length from the base, and each branch is subdivided 
into three tips; in the female the vulva is in the caudal half of the body; 
the eggs measure 52 to 61 p. in length and 42 to 38 /x in breadth; they are 
oval and have bluntly rounded poles. Both parasites inhabit the small 
intestine, especially the jejunum and ileum, but also the duodenum and 
occasionally the stomach. Infection may occur (1) through the skin, 
whence the larvae reach the circulatory system and eventually gain the 
small intestine; and (2) by way of the digestive tract with contaminated 
food or water or dirt on the hands. The eggs are oviposited in the 
intestine of the patient, but do not develop until after they escape with 
the feces. The conspicuous lesions consist of general anemia, deficient 
coagulability of the blood (due to a toxin produced by the hookworm), 
and catarrh of the intestinal tract. 

Symptoms. — The symptoms vary with the severity of the infection. 
Ova may be present in the stools without noteworthy symptoms. The 
chief manifestations consist of gastro-intestinal irritability, such as poor 
appetite, nausea, vomiting, epigastric distress, flatulence, etc.; slight 
fever; and in advanced cases secondary anemia, with high leukocytosis 
and eosinophilia. The patient tires readily and complains of lassitude. 
The liver and spleen may become enlarged ; the heart may become weak 
and dilated, and oedema may develop. The diagnosis is readily made 
by finding the worms or the ova in the stools. The outlook is favorable 
in early cases, but the mortality is about 30 per cent. 

Treatment. — Efforts should be made to minimize and prevent the 
infection by insisting upon the wearing of shoes in infected regions, 
examining the stools of persons in infected regions, and carefully destroy- 
ing contaminated stools, and disinfecting privies. The patient should 
be put on a fluid diet for a day; in the evening he should take a saline 
cathartic, but no food. In the morning an adult should be given 30 to 
45 grains (2 to 3 grams) of thymol (in cachets with an equal amount of 
milk sugar) , and at the end of three or four hours (earlier if symptoms 
of intoxication develop), he should take another saline cathartic. This 
may be repeated at the end of a week if worms or ova are still present. 
Beta-naphthol and male fern also have been recommended. The anemia 
requires the use of iron. 

Strongyloidosis. — Infection with Strongyloides stercoralis is common 
in tropical and subtropical zones (75 per cent, of the anemias of India) ; 
but it occurs also elsewhere, including the United States. Infection 
may occur through the skin, or by means of contaminated food or water. 
The parasite apparently may be harmless, or it may set up an intestinal 
catarrh and diarrhoea. The diagnosis may be made by finding the ova 
in the stools. Thymol, as in uncinariasis, is the best treatment, but it is 
not always efficacious, since the parasite may burrow into the tissues. 

Ascariasis (Eelworm Infection).— Infection with Ascaris lumbri- 
coides (Linnaeus) is widespread, but is most common in warm climates. 
It may occur at any age, but is most frequent in children. Several or 
many worms may be present in the one case. The male parasite 



220 METAZOAN INFECTIONS 

measures 15 to 17 even 25 cm. in length and about 3 mm. in diameter; the 
female, 20 to 40 cm. in length and 5 cm. in diameter, and is oviparous; 
they are grayish to reddish yellow in color; the anterior end is provided 
with three lips; the eggs are 50 to 75 by 36 to 55 a, unsegmented when 
oviposited, and provided with a thick mamillate covering, frequently 
tinged yellow when found in the feces. The parasites live in the small 
intestine. Development is direct, without an intermediate host. Infec- 
tion is acquired by contaminated drink, fruit, hands, etc. ; the fly may 
be an active agent in transmitting the infection. The embryo being 
swallowed develops directly into the adult worm. Symptoms may be 
entirely in abeyance, or there may be various ill-defined gastro-intestinal 
manifestations, or nervous symptoms in children, and eosinophilia. The 
disorder, of course, is recognized when a worm is passed by the rectum 
or is vomited. In other cases the ova may be found in the stools. The 
best treatment consists of the use of santonin, \ to 1 grain (0.03 to. 0650 
gram) to a child, 2 to 3 grains (0.13 to 0.20 gram) to an adult, with or 
followed by calomel, and later a saline cathartic. This may be repeated 
on the third and the fifth day. Thymol and oil of chenopodium also 
have been recommended. 

Oxyuriasis (Pinworm Infection; Threadworm Infection ; Seatworm 
Infection). — Infection with Oxyuris (Oxyurias) vermicularis (Linnaeus) 
is widespread, and very common in children and women. Few or many 
worms may be present in the one individual. The parasite is small, 
white, and round, and measures 3 to 5 mm. (male) to 10 mm. (female) 
in length and 0.16 to 0.6 mm. in diameter; the male has but one spicule; 
the female is provided with a relatively long, sharply pointed tail; the 
vulva is in the latter half of the anterior of the body; two uteri are present 
filled with numerous eggs; these eggs are 50 to 52 by 16 to 24 jn, and have 
a thin shell and a dorsal surface much more convex than the ventral. 
The fertilized females wander to the cecum, and later when gravid to 
the colon. Infection is acquired by auto-infection (infecting the finger 
nails by scratching the anus to relieve irritation occasioned by worms 
wandering from the rectum — the worm is thus often crushed); from a 
bed-fellow, or a nurse, or the bedclothes ; or from infected food or drink. 
Flies possibly transmit the infection to food, etc. Development is direct 
— without an intermediate host. Symptoms may be entirely in abeyance 
— in slight infections. In severe or heavy infections, gastro-intestinal 
symptoms are common, especially foul breath, abdominal distress, 
nausea, vomiting, diarrhoea, etc., as well as nervous symptoms, such as 
headache, restlessness, etc. The anus is often markedly irritated, 
and itches and burns, from out-wandering of the female parasite; 
these may invade the vagina, even the uterus and the peritoneal cavity. 
The diagnosis is readily made from detecting the worms in the stools or 
about the anus, or from finding the ova in the stools. The best treatment 
consists of santonin and calomel, as mentioned under ascariasis. Thy- 
mol, beta-naphthol, and a bitter infusion, such as gentian, have also been 
recommended. In addition, with a view to rid the rectum of worms, one 



NEMATHELMINTHIASIS 221 

should use daily, for a week or ten days, enemas of an infusion of quassia, 
or turpentine and water, or saline solution, etc. The itching about the 
anus may be relieved by belladonna or zinc oxide ointment. 

Trichocephaliasis (Whipworm Infection). — Infection with Trichuris 
trichiuria (Linnaeus) is widespread, and occurs in man, apes, etc. 
The parasite has the general form of a whip; the male measures 40 to 
45 mm. and the female 45 to 50 mm. in length; the eggs measure 50 to 
54 by 21 to 23 ,u, and are of a yellowish or dark brown color, with un- 
segmented protoplasm and a peculiar light spot at each pole resembling 
apertures. The parasites inhabit the cecum, but may be found in the 
appendix, colon, and ileum. Symptoms, as a rule, are entirely in abey- 
ance. In some cases a more or less well-marked secondary anemia 
results. Appendicitis is said to have been provoked by the worms, 
which also have been credited with transporting infecting bacteria 
(typhoid bacilli). The diagnosis is readily made by finding the worms 
or the eggs in the feces. The treatment is unsatisfactory: thymol and 
male fern have been recommended, as well as benzine internally and 
irrigations of the colon with benzine, 1 dram (4 c.c.) to a quart (liter) 
of warm water. 

Acanthocephaliasis. — Infection with Acanthocephali (thorn-headed 
worms) is of very little importance in human medicine. 

Trichinosis (Trichiniasis) . — Infection with Trichinella spiralis is 
widespread, and is found in man, hogs, wild boars, rats, dogs, and cats. 
Stiles states that three stages of the parasite should be clearly held in 
mind: (a) The adults live in the duodenum and jejunum; the males 
measure 1.4 to 1.6 mm. in length by 40 fi in diameter, while the females 
are 3 to 4 mm. long by 60 fi thick; they are circular on cross section, and 
appear as minute thread-like objects; the cesophagis is supported by a 
single row of cells known as the cell-body; the male is without spicules; 
the female is viviparous, the vulva being situated about one-fifth the 
length of the body from the mouth. The males die shortly after copula- 
tion. The females may remain for a few weeks in the lumen of the intes- 
tine, or they bore into the lymphatic spaces of the intestine where they 
live about five to seven weeks and deposit their numerous young, about 
1500 or more per female; (b) embryos, which measure about 90 to 100 fi 
in length by 6 p. in breadth; these wander, either with the lymph or with 
the blood, less frequently actively, to the striated muscles; they begin 
to reach the muscles about the tenth day after infection; they enter the 
muscle fibers and there develop into (c) encysted larvae; these cysts vary 
somewhat in size, but are usually about 400 by 250 //. The encysted 
larvae may remain alive in the muscles for years, cases being reported 
for as long periods as twenty to thirty-one years. The encysted worm 
(the "fleshworm") is the infecting stage, found in the hog; upon being 
swallowed in raw or rare pork, the cyst is destroyed, the larvae pass from 
the stomach to the small intestine and develop within about two days 
or less to the adults; the latter copulate and may have embryos in the 
uterus within less than a week after infection. Man becomes infected 



222 METAZOAN INFECTIONS 

from eating pork; hogs, from eating uncooked swill containing scraps 
of pork, or swine offal at country slaughter houses, or rats; and rats, 
from eating one another, scraps of pork in houses or meat-shops, and 
swine offal at country slaughter houses. 

Symptoms. — The symptoms may be slight and escape observation. 
Typical cases present Rupprecht's three more or less well defined periods, 
corresponding to the three stages of the parasite and their respective 
location: (1) The period of ingression, marked by predominance of 
gastro-intestinal symptoms — anorexia, nausea, vomiting, diarrhoea 
(usually profuse), sometimes succeeded by constipation, recurrent 
abdominal pains, vague pains in the muscles, a primary and transient 
cedema of the eyelids (about the eighth day), etc. (2) The period of 
digression, marked often by rather abrupt onset about the ninth to the 
fourteenth day (rarely later), fever, pain and tenderness of the muscles 
(especially the biceps and the gastrocnemius), which become firm and 
resistent, especially on motion; this, as a rule, is exceedingly painful, 
and may inhibit mastication, phonation, the movements of the eyes, 
respiration; indeed, dyspncea may become extreme and be associated 
with more or less violent asthmatic paroxysm. There is a marked 
leukocytosis (upward of 30,000) and a notable esosinophilia , (often 50 
per cent, of the leukocytes). (3) The period of regression, marked by 
exaggeration of all the symptoms; a second cedema, especially of the 
head ("big head"), may develop; anemia, emaciation, and a cachexia 
may supervene; or the parasites become encysted, the symptoms lessen, 
and the patient recovers. 

Diagnosis. — The diagnosis may often be suspected from the fever, 
transient oedema of the eyelids, and sore muscles. These with marked 
eosinophilia make the evidence almost if not quite conclusive. In addi- 
tion one should search for a source of infection, examine suspected pork 
for encysted larvae; and examine the patient's stools and blood for the 
adult worms, and a piece of excised muscle (gastrocnemius or deltoid) 
for the encysted larvse. 

Prognosis. — The outlook depends upon the severity of the infection. 
In general it is good, better in children than in adults. The mortality 
does not average over 5 per cent., although in some local epidemics it 
may be very high. 

Treatment .—The infection may be prevented by thorough inspection 
of pork at abattoirs, and by thoroughly curing and cooking all pork 
before it is eaten. If the infection is discovered or suspected early, the 
patient's gastro-intestinal tract should be thoroughly evacuated — by 
gastric lavage, and by calomel and saline cathartics. Perhaps thymol 
and beta-naphthol also might prove of service. Glycerin in large 
amounts has been recommended, in the hope that on account of its 
hygroscopic properties it may destroy the worms. Otherwise the treat- 
ment is symptomatic: hot applications or baths and morphine to relieve 
the pain, whiskey for its general supportive effect, etc. There is no 
known remedy that affects the parasite in the muscles. 



NEM AT HELMINTHIASIS 223 

Dracunculosis (Dracontiasis ; Guineaworm Infection; Medina- 
worm Infection). — Infection with Dracunculus medinensis (Linnaeus) is 
distinctly an Old World disorder, but occasional cases are observed in 
this country. The parasite is whitish or yellowish, 50 to 80 or more 
cm. in length, and 0.5 to 1.7 mm. in diameter; its anterior end is bluntly 
rounded, with a small terminal mouth and six papilla?. The uterus is 
enormously developed and filled with sharp-tailed embryos, 0.5 to 0.75 
mm. long by 0.17 mm. in maximum diameter. Infection is probably 
acquired through the drinking water; possibly by way of the skin. After 
copulation the male probably dies, and the female wanders to the sub- 
cutaneous tissues. The symptoms consist of the production, by the 
gravid parasite, of a small, painful, blister-like swelling, particularly on 
the feet and ankles; this ruptures, leaving an ulcer, at the base of which 
the head of the parasite may be seen; chills, fever, nausea, and vomiting 
may occur. Healing does not ensue until the parasite has been expelled. 
The treatment consists of the injection into the ulcer of mercuric 
bichloride (1 to 1000) or excision of the parasite. 

Filariasis. — Many filarial infections have been reported in man, but 
major interest centres in Filaria bancrofti (Filaria nocturna, Manson). 
The infection occurs in tropical and subtropical countries, but isolated 
cases have been observed in many regions of the temperate zone. The 
adult parasite, which occurs only in man, is a whitish or brownish, 
transversely striated worm, 44 to 95 mm. long by 0.1 to 0.26 mm. in 
diameter; the male has two spicules, 0.2 and 0.6 mm. long, an anogenital 
pore, 138 mm. from the tail; renal papillae are uncertain, but apparently 
there are three pairs of postanal papillse; the vulva of the female is 
0.66 to 1.2 mm. from the head, the anus 225 \l from the tip of the tail; 
viviparous. The larvae, which occur in a number of mosquitoes (Ano- 
pheles, Culex, Panoplites), are 300 to 340 p. long by 6.6 to. 8.5 or 11 n in 
diameter, and are provided with a sheath and sharply pointed tail. 
They are found in the circulating blood, and they show a more or less 
marked periodicity in that they are much more numerous during the 
night, but if sleep is reversed to the day-time, the periodicity also is 
reversed. Mosquitoes, while biting patients, swallow these larvae, which 
then undergo development in the muscles, and finally, after fourteen to 
seventeen days, or by lower temperature, up to thirty-five to forty-one 
days from the time of infection, the worms reach a stage in which they 
are transmitted to man during the bite of the mosquito. Manson states 
that the organism may produce abscess, lymphangitis, varicose groin- 
glands, varicose axillary glands, lymph scrotum, cutaneous and deep 
lymphatic varix, orchitis, chyluria, elephantiasis of the leg, scrotum, 
vulva, arm, mamma, etc., chylous dropsy of the tunica vaginalis, chylous 
ascites, and chylous diarrhoea. The blood may reveal a lymphocytosis 
(up to 40 per cent.) and an eosinophilia (up to 18 per cent.). The 
diagnosis may be made by finding the larval filaria in the blood, urine, 
or chylous accumulations. Preventive measures comprise killing and 
avoiding mosquitoes. The older view that the infection was acquired 



224 METAZOAN INFECTIONS 

from the drinking water suggested its being boiled, but this view has been 
abandoned. As far as is known, medicinal treatment is without much 
avail, although good results are said to have attended the use of thymol, 
ichthyol, etc. The patient should receive supportive treatment, and it is 
perhaps wise to limit the fluid intake and give purgatives from time to 
time. Surgical intervention is indicated in some cases. 

Filaria loa (diurna, Manson) is a small threadworm that circulates in 
the blood during the day, inhabits the connective tissues throughout the 
body, and is thought to be the cause of so-called Calabar swellings. 

Filaria perstans, of which only the larvae are known, is smaller than 
Filaria loa, and is said by Manson to be the cause of craw-craw, a papulo- 
pustular eruption of the West Coast of Africa; but like other filarial it 
frequently is found in the blood in the absence of noteworthy symptoms. 

Anguillula aceti (the vinegar-eel) and Leptodera pellio have been 
found in the human bladder and vagina; and Dicotophyme renale, the 
giant strongyle, or canine kidney-worm, has occasionally been found in 
man. 

ACARIASIS. 

(Acarine Infections.) 

Ixodiasis Tick (Infection). — There are two families of ticks 
(Ixodoidse) — Argasidse, in which the head is subterminal in the adult; 
and Izodidse, in which the head is terminal in the adult. The impor- 
tant species are Ornithodorus moubata, the agent active in transmitting 
Spirochseta duttoni, the cause of African tick fever (relapsing fever); 
Dermacentor venustus, Banks (andersoni, Stiles), and Dermacentor 
modestus (Banks), the agent active in transmitting the cause of Rocky 
Mountain spotted fever, or tick fever (which should not be confounded 
with the African tick fever); and Boophilus annulatus, the agent active 
in transmitting the cause of Texas fever. These and other ticks cling 
tenaciously to the skin, but on covering them with oil or vaseline (thus 
closing their breathing spaces) they release their hold and drop off. 

Sorcoptic Acariasis (Sarcoptic Itch). — Infection with Sarcoptes 
scabiei is universal, involving man and animals. The parasite, 
as it occurs in man, is whitish yellow, round to oval, with transverse 
rows of small spines, and a number of longer bristles; the male measures 
0.2 to 0.3 by 0.145 to 0.190 mm., and the female, 0.33 to 0.45 by 0.25 to 
0.35 mm.; they bore irregular galleries, 0.5 mm. to 4 to 5 cm. or more 
in length, in the epidermis, especially on portions of the body where the 
skin is thin and soft, as on the flexor surface of the carpus, between the 
fingers, in the groins, at the knee, on the penis, breast, etc., and at points 
subject to pressure, as at the waistband. The female is found at the 
blind end of the gallery; she deposits her eggs (15 to 50 in number) and 
feces as she progresses. The eggs measure 140 fi and hatch in four to 
eight days; the parasite becomes mature twenty-eight days after birth. 
The male dies shortly after copulation. Infection takes place directly 



PARASITIC INSECTS 225 

from person to person through prolonged contact, indirectly through 
bedclothes, towels, clothes, etc., or by direct contact in handling animals. 
The main symptoms consist of itching, increased by heat, exercise, and rest 
in bed; and a papular, vesicular, or pustular eruption, the result partly of 
scratching and partly of the mechanical and chemical irritation provoked 
by the parasite. The diagnosis is readily made by detecting the galleries 
with the female at the end. The treatment consists of thorough cleansing 
of the affected part with green soap and hot water; and thorough inunc- 
tion with mercurial ointment, sulphur ointment, or a compound naphthol 
ointment (naphthol, 15; prepared chalk, 10; green soap, 50; lard, 100; 
Kaposi). After the ointment has been allowed to act for four or five 
hours, the patient should take a warm bath and put on clean non- 
infected clothes. 

Other mites may cause various disorders, such as Demodex follicu- 
lorum, which, invading the hair follicles, may set up nodular formations ; 
Leptus americanus (irritans, autumnalis), the harvest mite, known also 
as the red bug, the harvest bug, or the jigger, which, burrowing into the 
skin of workers in the field in summer, may set up considerable irritation, 
and Pediculoides ventricosus, the cause of grain or straw-bed itch. 



PARASITIC INSECTS. 

Phthiriasis (Pediculosis). — There are three varieties of pediculidse — 
Pediculus humanus (capitis), the head louse; Pediculus corporis (vesti- 
menti), the body louse; and Phthirius pubis, the pubic louse. They 
are found only in persons of uncleanly habits. They cause irritation 
and itching and eczematous and pustular eruptions. The treatment 
consists of cutting the hair and saturating the infected parts with kero- 
sene, or with carbolic lotions (2 per cent.), which are more destructive to 
the eggs (nits). Mercurial ointment is serviceable in the event of pubic 
infection. 

Fleas. — Sarcopsylla penetrans (the burrowing flea, jigger flea, 
chigger) may burrow into the skin of the feet, but also elsewhere, and set 
up considerable irritation, suppuration, and ulceration. It should be 
taken out with a sharp knife; chloroform or mercurial ointment may be 
applied. Of jumping fleas, there are two that may attack man — Pulex 
irritans, the common or house flea, and Ctenocephalus canis, the cat and 
dog flea. These may act as ectoparasites, biting man; as an intermediate 
host for certain tapeworms; or as disseminators of plague. The house 
should be rid of fleas by sulphur fumigation, sprinkling about pyrethrum 
powder, or washing the floors with benzine or hot soapsuds. 

Bed-bugs. — Two types of bed-bugs infect dwellings — Cimex lectu- 
larius, the common bed-bug, and Conorhinus sanguisuga, the Mexican 
bed-bug. Stiles recommends fumigation with flowers of sulphur, 2 
pounds to 1000 cubic feet of space, as the best method of ridding a house 
of these pests. 
15 



226 INFECTIONS OF UNKNOWN ETIOLOGY 

Myiasis. — Compsomyia macellaria may deposit its eggs in wounds. 
The larva, known as the screw-worm, issues within a few hours, and may 
burrow into the tissues. Intestinal infection also may occur. Many 
other dipterous insects, mosquitoes, flies, beetles, etc., are of much and 
increasing medical importance, not so much because of the disorders 
that they may engender per se, but on account of the divers sorts of infec- 
tion that they transmit. They are of special importance in tropical and 
subtropical countries, where the control of many of the known and un- 
known or ill-understood infections unquestionably depends upon a study 
of the life habits and other biological characteristics of various sorts of 
insects that undoubtedly act as transmitting agents. 



INFECTIONS OF UNKNOWN OR DOUBTFUL 

ETIOLOGY. 



VARIOLA. 

(Smallpox; Varioloid.) 

Variola is an acute, specific, infectious, and highly contagious disease, 
characterized by high fever, usually of sudden onset and of characteristic 
course, and an eruption consisting successively of macule, papule, vesicle, 
pustule, and crust. 

Etiology. — Variola occurs at all ages (in the case of pregnant women 
sometimes implicating the foetus), and affects all races, and the sexes 
indiscriminately. It usually prevails epidemically, especially during 
the late fall, the winter, and the spring; but sporadic cases are often 
encountered. One attack usually confers immunity, but undoubted cases 
of second and even third attacks have been reported. Some few persons 
are apparently naturally immune. 

The exciting cause of the disease has not been isolated with certainty 
— although a number of supposedly causative microorganisms have been 
described. Recently some interest has been shown in the supposed 
etiological significance of a protozoon, Cytoryctes variola?, described 
originally by Guarnieri, later studied by Wasielewski, and more recently 
investigated by Councilman, Magrath, and Brinckerhoff — who, to- 
gether with Calkins, describe what they believe to be its life history. 
The streptococcus may be isolated from most of the lesions (primary, 
or essential, and complicating), and seems to bear some relation to at 
least certain phases of the disease. The contagium is present in the blood 
of the patient, the emanations and exhalations, the secretions and ex- 
cretions, and especially the dried crusts. The disease is highly con- 
tagious throughout its entire course (possibly even before the occurrence 
of the eruption). Practically all persons exposed are attacked, unless 



VARIOLA 227 

thev are immune naturally (very rare), by a previous attack, or by 
vaccination. Infection is transmitted by direct contact or proximity, 
by a third person, or by fomites, especially clothes and house furnishings, 
to which the contagium clings with extreme pertinacity, and for a long 
time. Recrudescence of the disease from year to year in places where it 
has been for a time endemic can almost always be attributed to such 
fomites, or to an ill-defined case. The question of the aerial convection 
of the infection is still debated, though certain facts speak in favor of it. 
An initial mild case, or even varioloid, may be the starting point of a 
virulent and widespread epidemic. Infection is acquired by inhalation. 

Pathology. — According to Councilman, Magrath, and Brinckerhoff, the 
specific lesion of variola (which is limited to the skin and the mucous mem- 
brane of the soft palate, pharynx, and oesophagus) consists of a focal, 
vacuolar degeneration of the stratified epithelium accompanied by serous 
exudation and the formation of a reticulum — which when fully developed 
constitute the characteristic multilocular pock, or pustule. In the skin 
the lesions begin with degeneration of the cells of the lower layers of the 
epidermis, accompanied by exudation, at first serous, later more or less 
cellular, the products of which are contained within the spaces of a reticu- 
lum formed by the degenerated cells. The exudate increases in amount 
and the spaces of the reticulum enlarge until its fibers finally rupture, 
and the lesion becomes a filled-out pustule. This development may 
take place wholly within the epidermis, and the fluid contents of the pock 
be separated from the corium by comparatively intact cells ; or the corium 
may form the bottom of the pustule, in which case there is usually necro- 
sis of the papillary border. (Edema, cellular infiltration, and hemor- 
rhage of the corium may occur. The subsidence and repair of the lesion 
are accomplished by the removal of the fluid portion of the exudate 
by absorption and drying, and by the regeneration of the epidermis, 
in the course of which the residual mass of degenerated epithelial cells, 
leukocytes, and debris, enclosed between two layers of horny epidermis, 
the old and the newly formed, is exfoliated. The lesions of the mucous 
membrane are proportionate in extent and severity to those of the skin, 
but on account of the absence of a horny layer of epithelium the degener- 
ated epithelial cells are cast off, and the vesicle within the epidermis 
is rarely seen, the pustule never. According to Councilman, Magrath, 
and Brinckerhoff the specific parasite of variola is found chiefly in 
the cells of the rete mucosum — its younger or cytoplasmic form in the 
protoplasm of the epithelial cells of early lesions and of such of the older 
lesions as are extending; its intranuclear form, for the most part, in 
more advanced lesions. According to the same authors, a constant, well- 
marked, and well-nigh characteristic lesion consists of proliferation within 
the hematopoietic organs, giving rise in the spleen, the lymph nodes, and 
the bone marrow to the formation of mononuclear, basophilic cells (which 
enter the circulation in large numbers), and in the lymph nodes and the 
marrow to phagocytic endothelial cells. Focal and interstitial cellular 
infiltration with mononuclear basophilic cells occurs constantly in 



228 INFECTIONS OF UNKNOWN ETIOLOGY 

the testicle, and usually in the kidney, the liver, and the adrenal glands; 
in the testicle (in consequence of pressure and thrombosis) it causes 
focal nercosis — apparently specific to variola. Focal degeneration, 
toxic rather than anemic, and leading to necrosis, at times with hemor- 
rhage, and accompanied by focal formation of phagocytic cells, is 
present in the blood-forming cells of the bone marrow, and constitutes 
a lesion almost pathognomonic. Diffuse toxic degeneration is present 
in the liver (where it is more marked than in any other infectious disease), 
the kidney, the adrenal gland, and the testicle. Toxic inhibition of cell 
differentiation is present in the bone marrow (absence of complete 
transformation of antecedent cells into polynuclear leukocytes) and in 
the testicle (absence of spermatogenesis). The paucity of polynuclear 
leukocytes in the specific lesions, in the focal degenerations, and in the 
bone marrow is so constant and so pronounced as to render it a strik- 
ing peculiarity of the disease. The common secondary infections, due 
commonly to pyococci, do not differ pathologically from similar lesions 
occurring under different circumstances. 

Symptoms. — The period of incubation is usually twelve days, though 
it varies from seven to fifteen days, and is commonly unattended by note- 
worthy prodromal symptoms (occasionally malaise). The onset is 
usually abrupt and quite characteristic, consisting of severe chills, high 
fever (103°, 104°, even 106° F.), severe lumbar pains, headache, and 
vomiting — which of themselves, in the presence of an epidemic, suggest 
the disease. Repeated chills or chilliness may occur within the first 
twenty-four hours. In children a convulsion not infrequently replaces 
the initial chill. In addition to the foregoing, in the early days of the 
disease, the patient is nervous and restless, his face is flushed, his eyes 
bright, and his skin hot and dry, though in some cases there is frequent 
and rather profuse perspiration; he complains of thirst, anorexia, and 
usually of constipation (though diarrhoea may be present in children); 
the pulse is rapid (100 to 140) and frequently dicrotic, and a systolic 
murmur, attributable to cardiac dilatation, sometimes develops; catar- 
rhal inflammation of the conjunctivae and of the respiratory tract (nose, 
throat, larynx, and bronchi) is rather common; and in many cases by 
the second or third day vertigo, stupor, or more or less delirium has 
developed. In severe cases coma and delirium may be initial symptoms. 
On the second day of the disease, in from one-sixth to one-fourth of the 
cases, so-called initial or prodromal rashes appear — measly, scarlatini- 
form, or petechial. Petechia? may occur either alone or with the measly 
or the scarlatinif orm rash. These, which often are quite indistinguishable 
from the ordinary rashes of measles and scarlatina, may be widespread, 
but they are usually localized to or involve especially the lower half of the 
abdomen, the outer aspect of the chest, the extensor and inner surfaces 
of the thighs and arms, and the natural folds of the body — the groins, 
axillas, elbows, etc. They usually fade at the end of twenty-four to 
thirty-six hours — except the petechise. 

The period of invasion lasts three days, at the end of which time, 



VARIOLA 



229 



that is, on the evening of the third day or the morning of the fourth, 
the temperature declines, the lumbar pains and the headache abate, the 
general condition of the patient improves markedly, and the true vari- 
olous rash appears. In mild cases the temperature may fall rapidly to 
the normal; in severe cases this also may happen, but often the tem- 
perature, although it lessens with the outbreak of the rash, does not 
approach the normal until after the lapse of twenty-four to forty-eight 
hours (Fig. 11). The rash develops first on the forehead near or in the 
hairy scalp and on the wrists, and then gradually spreads over the 
entire body and sometimes to the mucous membranes in contact with 
the air (mouth, nose, conjunctiva, pharynx, larynx, Eustachian tube, 
trachea, oesophagus, anus, vagina, urethra). It is, however, always 
more marked on the face, scalp, wrists, hands, and fingers, and is less 
where the initial rashes were most marked. It consists at first of 



Fig. 11 




Smallpox in an un vaccinated man, aged thirty-seven years, showing the temperature of the 
initial stage, the secondary or suppurative fever, and a later irregular fever, due to abscesses and 
cellulitis; recovery. (Welch and Schamberg.) 

small reddish, or rose-colored, macules, which on the first day give 
rise to papules that are quite hard, "shotty," and attended by intense 
itching. Sometimes they may be felt before they can be seen. The 
papules gradually enlarge, and at the end of two days (the fifth or sixth 
day of the disease) become vesicles— spherical, elevated, multilocular, 
and containing clear serum. By the following day well-marked central 
depression (umbilication) of the vesicles is usually apparent. By the 
eighth day the first pocks have become pustules, and by the tenth or 
eleventh day pustulation is usually complete — the pocks have become 
larger, have lost their umbilication, the contained fluid has become 
turbid (purulent), and they are surrounded by a halo of inflammation. 
Concurrent with the pustulation, the fever returns — so-called secondary 
or suppurative fever, which may reach 104° or 105° F., or more; the 
general symptoms become aggravated; pain, tenderness, and itching 
become almost intolerable, and the areas of skin intervening between 



230 INFECTIONS OF UNKNOWN ETIOLOGY 

the pocks become often extremely swollen and cedematous, so that the 
patient presents a most repulsive appearance; the cervical lymph nodes 
are usually much enlarged, and the spleen palpable; leukocytosis devel- 
ops; albumin and casts are present in the urine in about two-thirds of 
the cases; and severe nervous symptoms, such as delirium and coma, 
not infrequently supervene. In favorable cases, desiccation begins on 
about the twelfth day, and by the fifteenth day is usually far advanced 
on the face. Gradually all the pocks dry up, and, as a rule, by the 
end of three weeks desquamation is complete. With the beginning of 
desiccation the secondary fever subsides, that is, it does not remain high 
for more than twenty-four to forty-eight hours ; it gradually falls by lysis 
and reaches normal on or about the fifteenth day, and though irregular 
fluctuations may occur for some days, convalescence is now established. 
The amount and degree of pitting depend, as a rule, upon the severity 
of the infection, upon whether or not the skin papillae have been destroyed. 
As a rule, the pits are pigmented for some time, and gradually whiten. 
The hair commonly falls out, but is soon restored. 

In unfavorable cases, soon after pustulation occurs, a typhoid state 
with marked delirium usually develops; the pulse becomes rapid and 
feeble, coma, subsultus tendinum, etc., supervene, and with evidences 
of profound intoxication the patient dies. 

The pocks on the mucous membranes, as a rule, do not proceed to 
suppuration, but rather to the formation of small ulcers. By their presence 
in the nose they occasion manifestations of coryza; in the mouth, fauces 
pharynx, and oesophagus, sore throat and dysphagia; in the Eustachian 
tube, purulent median otitis; in the larynx, oedema, perichondritis, and 
sometimes laryngeal obstruction; in the trachea and bronchi, tracheo- 
bronchitis; in the conjunctiva, conjunctivitis, sometimes progressing to 
keratitis with perforation, panophthalmitis, etc. 

Varieties. — Several varieties of smallpox are described: (1) Discrete 
smallpox — in which the pocks are relatively few in number and discrete, 
and the general symptoms moderate in degree. (2) Confluent smallpox 
— in which the pocks are numerous and tend to coalesce, whence the 
greatest distortion of the countenance and limbs not infrequently occurs. 
Often the skin of the entire head and of the extremities becomes a large, 
superficial abscess. The general symptoms are severe — high fever, 
delirium, the typhoid state, etc.; death may ensue, or convalescence is 
prolonged. (3) Hemorrhagic smallpox : (a) in which the disease at the 
beginning pursues an ordinary course, but in which hemorrhages occur 
into the vesicles and pustules (variola hemorrhagica pustulosa). Death 
usually follows on from the seventh to the ninth day. Gradations, 
however, are observed between this type of the disease and the more mild 
cases, in which occasionally small hemorrhages occur into the pocks. 
(6) Petechial, black, or malignant smallpox (purpura variolosa), in which 
the blood dyscrasia is extreme, the initial rash markedly hyperemic 
(often purplish) and petechial; later the hemorrhages increase in size 
and involve the conjunctivae and the mucous membranes (hematuria, 



VARIOLA 231 

hematemesis, melena, menorrhagia, hemoptysis, etc.), the pulse becomes 
rapid, the respirations very much accelerated, and death often occurs 
as early as the third day — that is, before the true rash appears. (4) 
Varioloid, or modified smallpox, which occurs in persons that have been 
vaccinated. The initial manifestations are much like those of true 
smallpox (variola vera), though they are usually milder. The pocks 
are few in number, usually confined to the face and hands, and may not 
progress beyond the vesicular stage, though some of them may become 
pustular; there is little if any secondary fever, and rarely any scarring. 
(5) A verrucose form has been described — one in which the pocks 
dry up by the fifth or sixth day to a horny consistency — hornpox, wartpox, 
crystalline pox. (6) A variola sine eruptione has also been described; 
it is said to occur during epidemics, to affect young persons especially, 
and the initial manifestations (fever, headache, backache) only develop. 
It must be exceedingly rare, if it occurs at all. (7) Abortive cases, with 
severe initial symptoms, but subsequently a rapid favorable course. 

Complications. — Complications, considering the common severity of 
the disease, are singularly few, though certain of the more common 
lesions may become aggravated and constitute real complications, such 
as laryngitis (which may lead to oedema and necrosis), conjunctivitis 
(and keratitis), and secondary infections, especially of the skin (furun- 
cles, erysipelas, gangrene, etc.). Bronchopneumonia is common in the 
fatal cases. Pleuritis (often suppurative), otitis media, parotitis, orchitis, 
ovaritis, arthritis, and certain disorders of the nervous system attended 
by paralysis are sometimes observed. 

Diagnosis. — The initial symptoms, abrupt onset, with severe chill, 
high fever, vomiting, severe lumbar pains, and headache, especially 
during an epidemic, suggest the disease. While the initial rashes may 
cause confusion in some cases, measles may be excluded by the absence 
of prodromes, of coryza, of conjunctivitis, of cough, and of Koplik's 
spots, and scarlatina may be excluded by the absence of sore throat, 
of unduly rapid pulse, of the hyperemic punctate rash in the fauces, 
and by the less uniform distribution of the cutaneous rash. Difficulty 
is often experienced in distinguishing between smallpox and chickenpox, 
but smallpox is suggested by a longer prodromal period, severe initial 
symptoms, long preemptive stage, the abundance of pocks on the face, 
wrists, and hands (as contrasted with the trunk), by the hard and " shotty" 
character of the pocks which appear in one crop (within thirty-six 
hours), and are uniform in size, deep-seated, umbilicated, and multi- 
locular, and do not show different stages side by side (as in varicella), 
by the occurrence of secondary fever and of leukocytosis, and by the 
absence of a recent successful vaccination. Typhus fever may be 
distinguished by the special etiological factors, by the macular and 
later petechial character of the rash, which is usually most abundant 
on the chest and the abdomen, and by the absence of remission of the 
fever upon the appearance of the rash. In pustular syphilis there is a 
history of syphilitic infection from six months to two years previously; 



232 INFECTIONS OF UNKNOWN ETIOLOGY 

there are not the preemptive manifestations of smallpox nor remission 
of the fever upon the appearance of the rash (though there may be some 
neuromuscular pains and slight fever); the cutaneous lesions are poly- 
morphous ; the pustular syphiloderm has usually been preceded by macu- 
lar and papular syphiloderms ; the pustules are usually discrete, come 
out in crops, are more abundant upon the trunk (relative freedom of 
the face), are rarely as deep-seated as in smallpox, though they usually 
have an indurated base; and there are frequently other evidences of 
syphilis. Impetigo contagiosa begins as vesiculo-pustules (not papules), 
and enlarging by peripheral extension, the lesions sometimes attain 
the dimensions of a ten-cent piece. 

Prognosis. — The mortality varies much in different epidemics; it is 
commonly from 25 to 40 per cent, in unprotected individuals, but in 
recent years the disease seems to have become milder, or rather there have 
been many epidemics of mild smallpox. Severe, confluent, and hemor- 
rhagic forms, as well as milder but complicated cases (especially in the 
debilitated), are likely to terminate fatally. The mortality of varioloid 
is from 1 to 3 per cent. 

Treatment. — The patient must be isolated and the strictest measures of 
prophylaxis rigidly enforced (page 29) . During the fever period the patient 
should be confined to bed, and should have an abundance of fresh air 
and a light nutritious diet — small amounts at frequent intervals. Atten- 
tion to securing a sufficient diet is especially necessary during the later 
periods of the disease, when the abundant suppuration saps the vitality 
of the patient. Water should be given in large amounts — to relieve the 
thirst and to promote the elimination of the toxins by flushing the 
kidneys. The addition of the alkaline diuretics (potassium citrate, 
acetate, etc.) to the water subserves a useful purpose. 

In the absence of a specific, treatment is largely symptomatic and 
supportive. Morphine is of much service in relieving the early pains, 
and later in controlling the cutaneous irritation and consequent nervous 
unrest, as well as, sometimes, the delirium. Vomiting, if continued, 
may be relieved by cocaine, cracked ice, champagne, or dilute hydrocyanic 
acid. The fever often calls for a diaphoretic febrifuge mixture (spirit of 
nitrous ether and solution of ammonium acetate), and cold sponging (occa- 
sionally the cold bath), which is of excellent service not only in controlling 
the fever, but in alleviating the evidences of toxemia (delirium, prostra- 
tion, etc.). In some cases continuous warm baths (hours or days) are 
valuable. The throat pain may be relieved by cracked ice or orthoform 
lozenges (1 grain, 0.06 gram each). Stimulants (whiskey, brandy, strych- 
nine, etc.) are often required in the later stages of the disease. 

But little can be done to prevent pitting; puncturing the pocks, and 
the use of silver nitrate, carbolic acid, iodine, etc., for this purpose are 
almost if not quite useless. The use of hot or cold compresses, or of 
carbolized vaseline or oil is often grateful to the patient. Welch and 
Schamberg recommend painting the face once or twice daily with tincture 
of iodine. Crusts, when they form, should be kept moist by vaseline or 



VACCINIA 233 

oil, which not only relieves the cutaneous irritation, but also prevents the 
dispersion of the infectious flakes. During the whole course of the dis- 
ease the eyes and the mouth should be kept clean by the use of mild 
antiseptic lotions. The patient may be permitted to get out of bed as soon 
as the temperature is normal. Repeated bathing and the use of anti- 
septic soaps should be encouraged during convalescence. If pocks have 
occurred in the scalp, the hair should be cut very close. 

(Edema of the glottis may necessitate tracheotomy. The severer 
forms of smallpox require considerable stimulation, but it is doubtful 
whether ergot, iron, gallic acid, etc., that have been administered in the 
hemorrhagic forms have been of any real service. Most of the special 
forms of treatment advocated from time to time, including the red-light 
treatment, have not proved of service in the hands of impartial observers 
of large experience. 

VACCINIA. 

{Cowpox; Vaccination.) 

Vaccinia is an acute, specific, infectious, and highly contagious disease 
of bovine animals which, when inoculated into man (vaccination), 
produces fever, constitutional disturbance, and a specific eruption, con- 
sisting of papule, vesicle, pustule, and crust, and affords protection against 
smallpox. 

Etiology. — Since Jenner introduced vaccination, in 1796, there has been 
discussion as to its nature — whether cowpox is an independent disease 
or smallpox modified by transmission through the cow. The weight 
of evidence, however, tends to confirm Jenner's opinion that cowpox 
is modified smallpox, that, at least, both are descended from a common 
ancestor, since (1) smallpox and cowpox afford immunity, the one to the 
other, and (2) human smallpox virus when inoculated into cows has 
produced cowpox (though cows are often refractory), and the lymph 
from such cowpox vesicles when inoculated into man has produced vac- 
cinia, and occasionally even more or less generalized eruptions — which 
may be regarded as smallpox. Some support to this view is found 
also in the results (still awaiting confirmation) of the investigations by 
Councilman, Magrath, and Brinckerhoff regarding the supposed para- 
sites of smallpox and of vaccinia. The many examinations of vaccine 
lymph have not disclosed w T ith certainty the specific vaccine organism; 
divers cocci (including contaminating pyococci), bacilli (including 
occasionally contaminating tetanus bacilli), and certain supposed animal 
parasites have been detected by different observers. Whatever its exact 
nature, the virus is filtrable, and doubtless belongs to the class of ultra- 
microscopic organisms. 

Method of Vaccination. — Cow lymph alone should be used, and only 
that obtained from trustworthy sources. The use of human virus has 
deservedly fallen into disrepute. During recent years the use of glycerin- 
ated cow lymph has become widespread, but many competent observers 



234 INFECTIONS OF UNKNOWN ETIOLOGY 

still prefer the dried "points." Assuredly the lymph should be as free 
as possible from contaminating microorganisms — which has not always 
been the case. 

The arm (near the insertion of the deltoid muscle) or the calf of the 
leg (frequently in girls) is usually selected for vaccination. The skin 
having been cleansed with water and soap (no antiseptics, since they 
destroy the vaccine), an area one-eighth to one-quarter inch in diameter 
should be scarified with a sterile scalpel or needle so as to remove only 
the epidermis, whereupon the vaccine should be rubbed in. One should 
be careful not to draw blood. A single area for inoculation is suffi- 
cient, though many European physicians prefer several, as many as five. 
After the vaccine has dried it should be covered with an aseptic dressing, 
and the wound thereafter treated aseptically. Most of the cases of serious 
inflammation of the arm following vaccination are attributable to second- 
ary infection of the wound. 

Symptoms. — The period of incubation of vaccinia is usually about 
forty-eight hours, and is commonly unattended by symptoms. On the 
third day a papule attended by swelling, redness, induration, and a 
feeling of tension becomes apparent at the site of inoculation; by the fifth 
or sixth day this has developed into an umbilicated, multilocular vesicle, 
the contents of which are at first clear but soon become turbid. Gradu- 
ally the vesicle increases in size, and by the eighth day has reaced its 
maximum — when it is very itchy and surrounded by a wide zone of in- 
flammatory induration and oedema. By the eleventh or twelfth day the 
contents of the pock are distinctly purulent, and the inflammatory zone 
may be quite extensive; the adjacent lymphatics are swollen and tender 
and inhibit the motion of the limb; and rarely almost if not quite the 
entire limb is swollen, but this is a manifestation of secondary infection. 
Soon after the twelfth day the inflammatory phenomena begin to sub- 
side, and by the fifteenth day a dried crust has formed, which usually 
drops off during the early part of the fourth week, leaving a pitted scar. 

While the local lesions are at their height there is usually some eleva- 
tion of the bodily temperature (100° to 102° R), more or less malaise, 
slight headache, and occasionally chilliness. 

Sometimes the evolution of the pock is unusually delayed. In other 
cases what may be mistaken for the true pock develops very early, but it 
does not present the characteristic appearances (vesiculation and um- 
bilication) ; it soon drys, and by the seventh or eighth day the crust drops 
off. These so-called spurious vaccinations afford no protection against 
smallpox. In revaccinations the appearances of the pock are not 
infrequently atypical. 

Complications. — Acland has arranged the possible complications as 
follows: During the first three days — erythema, urticaria, vesicular and 
bullous eruptions, invaccinated erysipelas; after the third day and until 
the pock reaches maturity — urticaria, lichen urticatus, erythema multi- 
forme, accidental erysipelas; about the end of the first week — general- 
ized vaccinia, impetigo, vaccinal ulceration, glandular abscess, septic 



VARICELLA 235 

infections, gangrene; after the involution of the pocks — invaccinated 
diseases — syphilis. Complications, as a rule, are uncommon, the most 
common being septic infection attributable to lack of attention to the 
wound. Syphilis has rarely been transmitted, and, of course, never 
when cow lymph has been used. Tetanus has occasionally been trans- 
mitted, and has proved fatal. 

The time for vaccination is during the first or second year of life, 
or immediately after birth if an epidemic prevails. Revaccination 
should be done before or about puberty, and every five or seven years 
thereafter, or oftener if an epidemic prevails. 

The value of vaccination cannot be questioned — since where vaccina- 
tion and revaccination are most thoroughly carried out smallpox is least 
common or is never seen (as in the German army, whence it has been 
banished), and where vaccination is most lax smallpox finds its readiest 
victims and exerts its greatest ravages. 



VARICELLA. 

(Chicken-pox.) 

Chicken-pox is an acute specific, infectious, and moderately contagious 
disease, characterized by mild fever and a papulo-vesicular eruption. 

Etiology. — Chicken-pox is essentially a disease of childhood, occurring 
usually before the seventh year, and attacking the sexes indiscriminately. 
It is rather uncommon in very young infants, but is probably more 
common in adults than is usually supposed. The disease generally 
occurs epidemically, but sporadic cases are rather frequently encountered. 
One attack usually, but not always, confers immunity. 

The exciting cause of the disease has not been isolated, although it 
is unquestionably present in the skin lesions. Infection is usually trans- 
mitted by direct contact or proximity, but may be transmitted by a third 
person or by fomites. Infection is believed to be acquired by inhalation, 
and is much favored by previous ill health and overcrowding, such as 
obtains in asylums and some schools, etc. There is no longer any question 
of the non-identity of smallpox and chicken-pox — an attack of one of 
these diseases does not confer immunity from the other. 

Pathology. — The characteristic lesion is the papulo-vesicular eruption. 
The lesions of the internal organs are those common to most of mild 
infections and toxemias. 

Symptoms. — The period of incubation is commonly fourteen days, al- 
though it is said to vary from ten to nineteen days. The onset is usually 
mild in character and is often not preceded by prodromes, although 
slight fever, malaise, and slight pain in the back and legs may be present 
for a day; occasionally there are chilly sensations, and rarely convulsions. 
Often the rash, which comes out within the first twenty-four hours, is 
the first evidence of ill health. The rash appears first on the trunk 
(chest and back), but soon also on the neck, face, and forehead (near 



236 INFECTIONS OF UNKNOWN ETIOLOGY 

or in the hairy scalp), and is sometimes encountered on the oral, pharyn- 
geal, and laryngeal mucous membrane — even in some cases on the con- 
junctivae and the genital mucosa?. The rash consists of small, reddish 
papules which speedily (within several hours) develop into vesicles; in 
some cases the papular stage may be apparently absent. The pocks, as 
a rule, are roundish or ovoid in outline, vary somewhat in size, contain 
clear fluid (though it may be turbid), are rather superficial, sometimes 
(but not often) umbilicated, although as desiccation progresses they 
become flattened and even somewhat depressed in the centre; though 
sometimes situated upon a slightly hyperemic base, this is often wanting, 
the pocks resembling clear blisters such as might be caused by drops 
of boiling water, and a peripheral zone of infiltration is not encountered. 
During the course of the second day the contents of the pock often become 
seropurulent, especially in ill-nourished children and in consequence of 
secondary infection. The individual pocks usually reach maturity at 
about the end of two days, and at the end of the third or fourth day 
desiccation begins; a scab soon forms, and is shed, as a rule, within two 
weeks, without leaving a scar. The rash is usually discrete, rarely con- 
fluent, and in consequence of its coming out in crops from the first 
to the third day, all stages in its development may be seen side by side. 
Usually not more than a dozen pocks, there may rarely be several 
hundred. In a few cases a scarlatinous rash precedes the development 
of the pocks. The temperature which is highest on the second and third 
days (as the rash comes out), rarely exceeds 102° F., though in severe 
infections in debilitated children it may reach 104° F. It falls by lysis 
as the rash fades. Some glandular enlargement, especially of the neck, 
may be encountered. 

In unusual cases, the vesicles may become very large, forming bullae 
and resembling pemphigus (varicella bullosa); in other cases hemor- 
rhages into the cutaneous lesions and the mucous membranes occur 
(varicella hemorrhagica); and occasionally necrosis and gangrene about 
the pocks develop (varicella gangrenosa). 

Complications. — Nephritis and adenitis sometimes occur. Secondary 
infection of the pocks sometimes leads to suppuration and subsequent 
scar formation, and occasionally to rather extensive streptococcic infec- 
tion (erysipelas). Varicella is often associated with other infections 
(epidemically as well as individually), especially measles and scarlatina. 

Diagnosis. — Difficulty is sometimes experienced in distinguishing 
between varicella and mild smallpox, but varicella is suggested by a 
short prodromal period, the abundance of pocks on the trunk (as con- 
trasted with the face), the occurrence side by side of pocks in different 
stages of development (papule, vesicle, and crust), the apparent super- 
ficiality, bleb-like and unilocular character of the pocks, and a previous 
and rather recent successful vaccination. Impetigo, pustular eczema, 
etc., sometimes must be considered in the differential diagnosis. 

Treatment.— The treatment consists of isolation (for two or three weeks) 
and general hygienic management (page 29) . Carbolized vaseline or hot 






TYPHUS FEVER 237 



boric acid solution should be applied to the pocks if there is much irri- 
tation. Medicines are rarely required, but stimulants should be admin- 
istered to the weakly, and a generous diet is always advisable, especially 
during convalescence. 



TYPHUS FEVER. 

(Exanthema tic Typhus Fever; Spotted Fever; Jail Fever; Ship Fever; 
Camp Fever; Famine Fever.) 

Typhus fever is an acute, specific, infectious, and highly contagious 
disease, characterized by sudden onset, macular eruption, grave nervous 
symptoms, and a characteristic fever curve ending by crisis on or about 
the fourteenth day. 

Etiology. — Typhus fever seems especially prone to attack those of 
adult life, but age, sex, race, season, and climate have little if any 
etiological significance. Formerly a widespread disorder and frequently 
occurring epidemically in different parts of the world, the disease is now 
seldom encountered, although sporadic cases occur in large cities from 
time to time. One attack usually confers immunity. 

The exciting cause of the disease has not been isolated, although it 
it is probably present in the exhalations and evacuations of the patient, 
in the blood, the skin lesions, and the scales. Recently Krompecher, 
Goldzieher, and Argyan have described what they believe to be protozoa 
in the blood. The disease is extremely contagious, the contagium being 
transmitted directly, by a third person, and especially by f omites, such as 
clothes, bed linen, dishes, toys, etc., to which the contagium clings with 
extreme pertinacity. Anderson and Goldberger, and Ricketts and Wilder 
studying tabardillo, the typhus fever of Mexico, have transmitted the 
disease to monkeys; they have found that the virus is in the blood 
of the patient during the febrile stage, and that it is not filtrable; 
that monkeys that recover show an immunity comparable with that in 
man; and that the body louse (Pediculus vestimenti) may transmit the 
infection. The infection probably may also be acquired by inhalation, 
since physicians, nurses, and attendants upon the sick during epidemics 
are very likely to contract the disease. The likelihood of infection is 
increased by general insanitary practices, destitution, and overcrowding 
such as obtain in tenements, asylums, jails, ships, camps, etc. 

Pathology. — There are no characteristic anatomical lesions, the lesions 
present being those common to most severe toxemias. Thus, the spleen 
is moderately enlarged and soft; the liver, kidneys, heart, voluntary 
muscles, nerves, etc., reveal parenchymatous and granular degeneration 
and necrosis; and there are marked hemolysis, subcutaneous petechial 
hemorrhages, and bronchial catarrh. 

Symptoms. — The period of incubation varies from seven to twenty-one 
days, being usually twelve days. In some cases there are prodromal 
symptoms lasting a day or two, and consisting of general malaise, loss 



238 



INFECTIONS OF UNKNOWN ETIOLOGY 



of appetite, headache, vertigo, and sometimes coryza. The onset of 
the disease is usually sudden, and manifested by chill, high fever, head- 
ache, pains in the back and limbs, prostration, and sometimes vomiting. 
The temperature may reach 104° to 105° F., by the end of twenty-four 
or thirty-six hours, and it continues high with slight morning remissions 
(Fig. 12). The chill may recur for a day or two. With continuance 



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The temperature in typhus fever, showing the decline by crisis. (Doty.) 



of the high fever, marked nervous manifestations referable to toxemia 
soon appear, such as severe headache, vertigo, tinnitus aurium, spots 
before the eyes, etc. The patient becomes dull and listless, sometimes 
wildly maniacal. There is much thirst, the bowels are confined, and the 
urine is concentrated and may contain a small amount of albumin. 

On the fourth or fifth day, by which time the temperature has reached 
its maximum, often 106° F., the characteristic eruption makes its appear- 
ance, first on the anterior fold of the axillse, and the wrists, or the backs 
of the hands, then on the sides of the abdomen and chest, and finally 
on the trunk, including the back and the extremities, but being rare on 
the face. It is made up of two elements — rose-colored or dusky macules 
superimposed upon a subcuticular mottling, whence it much resembles 
measles, and has been spoken of as the mulberry rash of typhus fever. 
It comes out rapidly, within twenty-four hours usually, and not in crops 
as does the rash of typhoid fever. At first the macules, which fade 
almost imperceptibly into the surrounding mottling, disappear upon 
pressure, but they soon become darker and less deleble, and later (eight 
to tenth day) become hemorrhagic (petechia?). The rash is rarely missed, 



TYPHUS FEVER 239 

except perhaps in the mildest cases, in which, however, it is largely 
petechial. 

During the course of the second week, concurrent with the change in 
character of the rash, profound toxemia (the typhoid state) develops. 
Delirium, often noisy at first, but later usually milder, muttering, and 
attended by sleeplessness, stupor (coma vigil), subsultus tendinum, and 
carphologia, continue. Prostration is extreme, and face expressionless 
and flushed, the pupils contracted, and the eyes injected. The tempera- 
ture, though somewhat lower than during the first week, continues high 
(102.5° to 103.5° F.), the pulse is weak (120 to 130 per minute), small, 
and often irregular and dicrotic. The apex beat and the heart sounds 
are weak, and a soft, systolic murmur is common. There may be a slight 
leukocytosis. The tongue becomes dry and fissured, and later sordes 
collect on the lips, gums, teeth, and tongue. The breath and the body 
generally are malodorous (by some said to be characteristic). Bronchitis 
continues, and with failure of the heart, hypostatic congestion of the 
lungs may develop. The urine is usually concentrated and contains 
a little albumin, lessened chlorides, and is frequently voided involun- 
tarily, although it may be retained. The spleen is usually enlarged and 
palpable. Bed sores not infrequently develop. In unfavorable cases, 
death ensues from exhaustion due to toxemia or from complications, the 
temperature often rising just before death to 108° to 109° F. 

In favorable cases at the end of the second week, usually on the 
fourteenth day, and sometimes preceded by a precritical rise, the tem- 
perature falls by crisis, within twelve to twenty-four hours, to normal 
or below, the patient sweats profusely, toxemia lessens, the general 
symptoms improve, and convalescence ensues. 

Varieties. — Mild and severe are sufficiently descriptive of the majority 
of cases. In certain abortive cases, the crisis occurs early and the 
eruption and delirium are not marked. In certain malignant or fulmin- 
ating cases (typhus siderans) death ensues early under manifestations 
of profound toxemia, marked delirium, high fever, cardiac collapse, 
and degeneration of the viscera. In some cases the disease is protracted, 
the fever and other manifestations extending into the third week. An 
afebrile typhus fever has been described. Relapse is very rare. 

Complications and Sequels. — Bronchitis, hypostatic congestion of the 
lungs, and bronchopneumonia are common. Gangrene of the lung some- 
times develops. Thrombosis and embolism with consequent infarction 
of the viscera and gangrene of the extremities occur. Extensive 
gangrenous bed sores, suppuration of the glands and of other tissues, due 
to secondary infections, furunculosis, parotitis, meningitis, hemolysis, also 
have been observed. Hemiplegia or monoplegia, the result of throm- 
bosis or embolism, and paralysis due to neuritis, sometimes follow. 
Rarely various forms of insanity persist for some time. 

Diagnosis. — In cases of moderate severity, the diagnosis is apparent 
from the presence of an epidemic, exposure to infection, characteristic 
onset, high fever, and characteristic rash. The recognition of mild 



240 INFECTIONS OF UNKNOWN ETIOLOGY 

cases, in the absence of an epidemic, requires a knowledge of the entire 
clinical course. Typhus, as contrasted with typhoid fever, is distin- 
guished by a sudden onset with chill, high initial and more continued 
temperature, early prostration, severe nervous symptoms (delirium, 
stupor), a characteristic petechial rash (with diffuse mottling), more 
likely injection of the sclerotics, and the termination by crisis on or 
about the fourteenth day, and by the absence of abdominal symptoms, 
the presence of the Gruber-Widal reaction, typhoid bacilli in the blood, 
feces, urine, and rose spots. Cerebrospinal meningitis, measles, small- 
pox, uremia, purpura, acute infective endocarditis, and malaria have 
more or less resemblance in certain minor or major points to typhus 
fever, but regard for the clinical manifestations of each disease should 
soon settle the diagnosis. 

Prognosis. — The mortality rate in epidemics varies from 10 to 20 
per cent. The extent of the rash is said to bear a direct relation to 
the severity of the infection. Unfavorable signs are hyperpyrexia, 
extreme toxemia, and the different complications. The young usually 
recover. 

Treatment. — The treatment in general does not differ from that of 
typhoid fever. The strictest isolation, thorough disinfection, and free 
ventilation (treatment in the open air), are imperative (page 29). The 
general management comprises the use of hydrotherapy and stimulants — 
hydrotherapy by sponging or bathing, large amounts of water to the 
patient to drink (much overlooked because of the stupor), and enteroclysis 
and hypodermoclysis to promote the elimination of toxins. Stimulants 
comprise the sponging and bathing just mentioned, alcohol (especially 
in subjects over twenty years of age), and strychnine, ammonium 
carbonate, camphor, etc. Coal tar derivatives should be avoided 
on account of the cardiac weakness. The food must be nutritious, 
easily digestible, given at stated intervals, bearing in mind that if we 
can support the patient for a stated time he is likely to recover from 
the self-limited disease. The complications are to be treated on 
general principles. 

SCARLET FEVER. 

(Scarlatina ; Scarlet Rash.) 

Scarlet fever is an acute, specific, infectious, and highly contagious 
disease, characterized by high fever, rapid pulse, sore throat, an ery- 
thematous rash, and a marked tendency to nephritis. 

Etiology. — Scarlet fever is essentially a disease of childhood, attacking 
the sexes equally, and being especially prevalent before the tenth year 
(90 per cent, of all cases). It is rare in young infants, but more common 
in non-immune adults. The disease is endemic in most large cities 
and frequenty prevails epidemically, especially during the fall and 
winter. One attack usually confers immunity, although recurrences are 
observed. Some persons are naturally immune to the disease, 



SCARLET FEVER 241 

The exciting cause of the disease has not been isolated with certainty. 
Many observers view the disease as a modified streptococcic infection ; 
the streptococcus may be isolated from most of the lesions, and assuredly 
plays an important part in the affection. Mallory has described a pro- 
tozoan-like organism between the epithelial cells of the epidermis, and 
Duval has found the organism in blister-serum; but the proof is not 
yet conclusive that this is the specific infectious agent. The blood, 
nasopharyngeal and oral discharges, epidermic scales, and urine are 
infectious. The disease is highly contagious and spreads with rapidity, 
though not as rapidly or widely as measles. Infection in the great ma- 
jority of cases is transmitted by direct contact or proximity to a patient, 
or a "carrier;" or by means of infected food, such as milk (responsible 
for a number of epidemics); occasionally by a third person, or by 
fomites. Infection is usually acquired through inhalation, sometimes 
through swallowing, and wounds. Patients with surgical wounds and 
puerperal women appear to be very susceptible to the infection, though 
most of the cases of supposed scarlatina described in such subjects are 
instances of streptococcic or staphylococcic infection. 

Pathology. — Scarlatina is devoid of characteristic lesions. The 
lesions in the nasopharynx are those of inflammation and ulceration; 
those in the skin, of hyperemia, which disappears after death. The 
lesions in the internal organs are those common to most toxemias, with 
sometimes special characteristics due to the frequent association of 
the streptococcus. The kidneys frequently show a rather characteristic 
lesion — a glomerulonephritis, though diffuse and hemorrhagic nephritis 
also occurs. Catarrh of the gastro-intestinal mucous membrane is com- 
mon; the lymph nodes", especially those of the neck, not infrequently 
suppurate; and fibrinopurulent inflammation of the serous membranes 
is often encountered in fatal cases. 

Symptoms. — The period of incubation is from one to seven days, 
usually from two to four days. The invasion is sudden — prodromal 
symptoms being entirely in abeyance or consisting merely of slight in- 
disposition. The initial symptoms, which are quite characteristic and of 
themselves suggest the disease, consist of nausea, vomiting, high fever, 
104° to 105° F. (Fig. 13), sore throat with pain on swallowing, swelling and 
tenderness of the glands at the angles of the jaw, and an unusually rapid 
pulse (140 to 180 per minute). Occasionally there is an initial chill; 
more often chilliness. Convulsions are common in young children. 
The throat is found to be acutely inflamed — the fauces, soft palate, and 
pharynx revealing a diffuse hyperemic redness and a fine, punctiform 
rash (even before the skin rash appears). 

On the second day, often even within the first twenty-four hours, the 
characteristic rash appears — first on the neck and chest and then (within 
twenty-four hours) rapidly spreading over the entire body. This con- 
sists of a multitude of minute red points, for the most part corresponding 
with the points of emergence of the hairs, set in the diffusely hyperemic 
and slightly swollen skin. The hyperemic areas are usually confluent 
16 



242 



INFECTIONS OF UNKNOWN ETIOLOGY 



and impart to the patient's skin an appearance suggesting a boiled lobster. 
The eruption is distinctly punctate in character — a character the more 
apparent the less the diffuse hyperemia; hence during the later stages 
of the disease. It disappears temporarily on pressure, and is usually 
most marked at the natural folds of the body — the groins, the bends of 
the elbow, the axill?e, and often on the lower part of the abdomen and 
on the inner aspects of the thighs. As contrasted with measles the face 
is often relatively unaffected. 

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The temperature in scarlet fever, showing the decline about the fourth or fifth day, and a sub- 
sequent rise and irregularity, due to nephritis and swollen glands. (Musser.) 



On the third day of the eruption, that is, at the end of about forty- 
eight hours, the disease is usually at its height. The fever remains 
high (104° to 105° F.) with slight morning remissions, the pulse frequent 
(140 to 160 per minute), and the entire integument presents a diffuse, 
bright scarlet hue (that serves to distinguish scarlatina from other 
exanthemas). The concomitants of fever and the expressions of 
toxemia are usually well marked : the patient is delirious at night and at 
least stuporous during the day, and the urine is reduced in amount, 
concentrated, of high specific gravity, and may contain a little albumin. 
The tongue, at first red at the tip and edges and covered on the dorsum 
with a grayish-white fur, through which the swollen papillae project 
(strawberry tongue), soon loses the fur and frequently also the super- 
ficial epithelium, and presents a swollen, red, and irregular surface 
(raspberry tongue). The fauces exhibit different grades of inflamma- 
tion: in the one case slight hyperemia with a punctate rash; in another 
case, a more severe inflammation especially of the tonsils, possibly a 
follicular tonsillitis; and in another case, pseudomembranous inflamma- 



SCARLET FEVER 243 

tion with more or less extensive induration and suppuration of the 
adjacent tissues. The glands at the angle of the jaw, swollen in all cases, 
frequently become exquisitely tender and may suppurate. The appetite 
is lost. The spleen may be palpable. Leukocytosis is common and 
may be marked. 

Having lasted four or five days (in mild cases, two or three days), the 
rash begins to fade, the throat manifestations abate, and the fever falls 
by lysis — reaching the normal, in moderately severe cases, by the eighth 
or ninth day — in mild cases earlier, in severe cases and in the event of 
complications, later. The subsidence of the rash is followed by a branny 
or flaky desquamation, which begins (as did the rash) on the neck and 
chest, and is usually proportionate to the severity of the rash. In severe 
cases veritable casts of the hands and feet may be shed; sometimes even 
the hair and nails are lost. Desquamation is usually complete at the 
end of fifteen or twenty-days, but may be prolonged until the seventh 
or eighth week. 

Varieties. — Depending upon the severity of the infection, the following 
varieties of scarlatina may be recognized: 

1. Mild scarlatina, in which the general and local symptoms are mild, 
and in which the rash is slight and lasts but a day or two. In some cases 
it may be absent — scarlatina sine eruptione. In some cases the nature 
of a mild sore throat is unsuspected until the skin desquamates, or until 
nephritis develops, or until an epidemic attributable to it ensues. 

2. Severe scarlatina, in which the general and local symptoms are 
severe: sudden onset, high fever (108° F.), scanty albuminous urine, 
marked prostration, severe nervous manifestations, headache, rapid 
feeble pulse, heart weakness, delirium, convulsions, coma, etc. — the so- 
called atatic form. This form, the expression of severe toxemia, is 
frequently fatal within a day or two — in some cases even before the 
appearance of the rash (during the period of invasion). 

3. Malignant scarlatina, of which we may distinguish: (a) The 
hemorrhagic form — in which hemorrhages occur into the mucous mem- 
branes and the skin. Often the hemorrhages are petechial, but fre- 
quently ecchymoses, involving large areas, develop ; and epistaxis, hemop- 
tysis, hematuria, etc., may occur. Intoxication is severe and death 
usually results on the second or third day. (b) The anginose form — in 
which the throat symptoms assume the predominance. Ulcerative 
and pseudomembranous inflammation of the tonsils and fauces, with 
marked fetor, induration and suppuration of the adjacent cellular and 
lymphatic tissues ensue. The lesions may spread to the nose and the 
larynx, leading to death from asphyxia; or the cellular inflammation 
may become widespread, and lead to Ludwig's angina, or perforation of 
the carotid artery, etc. Otitis media is common. Bacteremia is the 
rule, and death speedily follows in most cases. The throat lesions, fre- 
quently diphtheroid, may sometimes reveal the Klebs-Loeffler bacillus. 

The rash sometimes exhibits peculiarities. Instead of becoming 
diffuse, the hyperemic areas may remain discrete — scarlatina maculosa; 



244 INFECTIONS OF UNKNOWN ETIOLOGY 

sometimes papular elevations occur — scarlatina papulosa; sometimes 
sudaminal vesicles appear— scarlatina miliaris; the vesicles may become 
purulent — scarlatina pustulosa; or large blebs may form — scarlatina 
pemphigoidea. 

Complications and Sequels. — The most important complications and 
sequels are nephritis and inflammation of the serous membranes. In 
addition to the albumin present in most cases and attributable to the 
toxemia, a true nephritis may occur. It may develop during the course 
of severe cases, but is quite common after mild cases, especially during 
convalescence (third or fourth week) — postscarlatinal nephritis. The 
onset is usually manifested by dropsy, but sometimes by lessening in 
the amount of urine or by uremia. The oedema often goes on to ana- 
sarca and effusions within the serous cavities and the meninges. These 
may lead to death, but usually recovery ensues after several weeks, 
although convalescence may be protracted for several months. An 
oedema without nephritis, and attributed to impoverishment of the 
blood, has been described! A septic nephritis, as part of a general 
pyemia, sometimes occurs. Chronic nephritis rarely develops out of the 
acute lesions, but the kidneys may remain susceptible for a long time, 
and in later life exposure to appropriate etiological factors may result in 
the ready production of a serious and even fatal nephritis. 

Of the inflammations of the serous membranes, pleuritis and 
pericarditis are common, and usually fibrinopurulent in character. 
Simple and malignant endocarditis, as well as myocarditis, may occur. 
Meningitis may develop and remain for a time unsuspected, especially 
in the event of convulsions. Pains in the joints are not uncommon — 
scarlatinal synovitis (miscalled rheumatism). Usually, an expression 
of the toxemia, the pain subsides with the toxemia; occasionally it persists 
longer, and the lesions may go on to suppuration (usually mono-articular). 
An associated chorea has been observed. Suppurative otitis media, the 
result of extension of inflammation along the Eustachian tube is common, 
and answerable for much of the deafness of later life. If neglected it 
may lead immediately to mastoid disease, sinus thrombosis, cerebral 
abscess, etc. An otorrhoea or rhinorrhoea persisting after apparent 
convalescence, even if non-purulent ("chronic carriers"), is answerable 
for the propagation of the disease and even for some epidemics. Sup- 
purative adenitis, especially of the neck, is rather common. Sudden 
death from acute cardiac failure sometimes occurs during convalescence. 

Concurrent infections are not infrequent — especially diphtheria, 
chicken-pox, measles, pertussis, erysipelas, typhoid fever, etc. 

Diagnosis. — The diagnosis is usually easy. The short period of incuba- 
tion, the characteristic initial symptoms, especially the early sore throat, 
the vomiting, the rapid pulse, the punctate hyperemia of the mucous 
membrane of the mouth and fauces, followed by the characteristic skin 
eruption, serve to exclude other diseases. From measles scarlatina 
may be excluded by the sore throat (as contrasted with general catarrhal 
symptoms), shorter preemptive period, the punctiform rash in the throat, 



SCARLET FEVER 245 

the absence of the Filatow-Koplik's spots, the more uniform erythematous 
rash (as contrasted with the blotchy or mottled rash of measles), the 
relative freedom of the face, the raspberry tongue, the undue accelera- 
tion of the pulse, and the presence of leukocytosis. In rotheln, the onset 
is less abrupt, there is rarely initial vomiting, the fever is less high, the 
pulse is less rapid, the rash is not punctiform, there is no raspberry tongue, 
the general symptoms are less marked, and there is little tendency for 
the development of nephritis. In scarlatina the throat lesions sometimes 
become "diphtheroid," and may not be distinguishable from those of 
true diphtheria, except by bacteriological examination. Diagnostic 
difficulties are sometimes enhanced by an erythematous rash that 
occasionally occurs in diphtheria. However, this is uncommon, and 
is darker and of shorter duration than the true scarlatinous rash, and 
is usually confined to the trunk. The two diseases not infrequently 
co-exist. In acute tonsillitis there is rarely an erythematous rash, but 
this is not punctiform, there is no raspberry tongue, no undue accelera- 
tion of the pulse, and no epidemic. Acute exfoliative dermatitis is often 
difficult of differentiation, but is suggested by absence of throat symp- 
toms and of the characteristic tongue, and by the rather marked tendency 
to recurrence, the earlier commencement of desquamation (even before 
the eruption has faded), the frequent involvement of the hair and the 
nails, and the comparative rarity of involvement of the kidneys. Drug 
rashes sometimes follow the administration of belladonna, quinine, 
potassium iodide, antitoxic serums, etc., and ptomaine rashes may 
occur after the use of tainted oysters, fish, etc., but these rashes are 
usually slight and transient (though they may be diffuse and marked), 
they are not punctiform, and there are none of the characteristic symp- 
toms of scarlatina. 

Prognosis. — The mortality varies much — from about 5 per cent in the 
mildest epidemics to 30 per cent, in the more severe. The death rate is 
higher the younger the child, and in general the poorer the social condi- 
tions. Unfavorable symptoms in individual cases are high fever, marked 
toxemia (delirium, etc.), hemorrhages, severe throat lesions, laryngeal 
obstruction, and nephritis. 

Treatment. — The patient must be isolated and the usual prophylactic 
measures enforced (page 29). Specific therapy is still a hope of the 
future. Some good results have followed the use of a polyvalent anti- 
streptococcic serum. More recently streptococcic vaccines have been em- 
ployed for prophylactic and curative purposes — with encouraging result. 
In the absence of specific treatment, the special function of the physician is 
to guide the child through the attack, and to prevent the development of 
complications. Mild cases, as a rule, pursue a favorable course under the 
beneficent influence of rest in bed, flannel garments (to lessen the likeli- 
hood of chill), an abundance of fresh air, a milk diet, considerable water 
(to promote the elimination of toxins), and regulation of the bowels. 
In all cases it is wise to insure a daily evacuation of the bowels, to 
administer a mild diuretic and diaphoretic febrifuge mixture (such, 



246 INFECTIONS OF UNKNOWN ETIOLOGY 

for instance, as is given on page 250), to give the child a warm bath 
twice daily and to follow this by oil inunctions. In the event of high 
fever and delirium, an ice bag should be applied to the head, and the 
bathings should be more frequent (every three hours). The bathing 
is much preferable to the use of antipyretic drugs. An alcohol rub at 
night often promotes a restful sleep. Stimulants (brandy, whiskey, 
strychnine, ammonium preparations, etc.) are called for in the event 
of marked toxemia (prostration, marked delirium, subsultus tendinum, 
the typhoid state, coma, etc.). The bromides are often serviceable 
in the wakefulness that sometimes attends the nervous irritability. 
J. C. Wilson recommends the routine use of chloral, in dosage sufficient 
to produce light somnolence, believing that it promotes diuresis and 
lessens the likelihood of nephritis, favorably modifies the nervous mani- 
festations, and allays the itching. Robert Milne recommends thorough 
rubbing of the body, from the crown of the head to the soles of the feet, 
morning and evening, for the first four days, and then once daily until 
the tenth day, with 10 per cent, eucalyptus oil; and swabbing the throat, 
every two hours, for the first twenty-four hours, with 10 per cent, car- 
bolic-acid oil — stating that this treatment modifies the severity of the 
attack, prevents nasal, oral, and renal complications, and abolishes the 
infectivity of the disease. 

The throat manifestations, as a rule, do not call for special treatment, 
but cleansing preparations should always be used — to reduce if possible 
the bacterial content of the throat, but more especially to remove all 
secretion that may tend to obstruct the inlet to the Eustachian tube 
and thus favor the development of middle-ear disease. Normal salt 
solution, Dobell's solution, hydrogen peroxide (15 per cent), potassium 
chlorate (2 per cent.), or potassium permanganate (2 per cent.), may be 
used for this purpose. Many physicians are partial to the use of iron 
which may be employed as follows : Tincture of iron chloride (J ounce, 
15 c.c), glycerin (J ounce, 15 c.c), and water (1 ounce, 30 c.c). 10 to 
15 minims of carbolic acid may be added to the mixture. In severer 
cases Loffler's solution is serviceable: Menthol, 10 c.c; toluol, 36 c.c; 
tincture of iron chloride, 4 c.c; and absolute alcohol, 60 c.c. This may 
be applied by means of a cotton swab. Should cultures from the throat 
reveal the diphtheria bacillus antidiphtheritic serum should be used 
without delay. 

During desquamation the child should be bathed daily with warm 
water and an antiseptic soap and then annointed with vaseline or oil. 
Especial attention should be paid to the ears, and in the event of pain 
appropriate measures, including early puncture of the drum membrane, 
should be instituted so as to obviate, if possible, deafness in later life. 
Iron and the bitter tonics are useful during convalescence. The child 
should be confined to the bed for at least ten days after the temperature is 
normal. During the entire convalescence one should always be guided 
by the knowledge that nephritis may develop (after exposure) three or 
more weeks after the temperature has reached the normal, and that the 



MEASLES 247 



child is perhaps infectious as long as there is any desquamation and cer- 
tainly as long as a naso-pharyngeal or aural discharge persists. The 
complications are to be treated on general principles. 



MEASLES. 

(Morbilli; Rubeola.) 

Measles is an acute, specific, infectious, and highly contagious disease 
characterized by catarrhal inflammation of the conjunctivae and the 
respiratory mucous membrane, fever, and a peculiar maculopapular 
rash. 

Etiology. — Measles is essentially a disease of childhood, attacking the 
sexes equally, and being especially prevalent between the second and the 
eighth year. It is unusual under six months of age, but it is more common 
in non-immune adults than certain other infective diseases, such as 
scarlatina. Recurrences are not uncommon, but one attack usually 
confers immunity. In many large cities the disease is endemic, and it 
frequently prevails epidemically, especially during the fall and winter. 

The exciting cause of the disease has not been isolated, although it 
seems to be present in the emanations from the patient, especially the 
breath, the nasopharyngeal secretions, and the desquamations. The 
disease is highly contagious and spreads with extreme rapidity. Infec- 
tion may be transmitted directly, or by a third person, or by fomites. 
It is acquired through inhalation, and is much favored by overcrowding, 
such as obtains in close, unsanitary dwellings, school-rooms, etc. 

Pathology. — Measles is devoid of characteristic lesions. Catarrh of the 
conjunctivae and the respiratory mucous membrane and hyperemia of 
the skin with slight if any cellular exudation occur. In severe and fatal 
cases bronchopneumonia, capillary bronchitis, atelectasis, pleuritis, and 
swelling of the bronchial lymph nodes and of the mucous membrane of 
the gastro-intestinal tract may be encountered. 

Symptoms. — The period of incubation is from seven to fourteen or 
eighteen days, the average being about ten days. The invasion, usually, 
is rather abrupt, with chilliness (or convulsions or vomiting in infants) 
moderate fever, 101° to 102° F. (Fig. 14), well-marked coryza, and 
catarrhal inflammation of the conjunctivae and the respiratory mucous 
membrane. The child appears to suffer from a cold in the head. It has 
a profuse nasal discharge, its eyes are injected, it complains of headache, 
photophobia, lacrymation, and sneezes frequently. Within twenty-four 
hours, as a result of extension of the catarrhal inflammation to the 
pharynx and bronchi, a cough develops. The fever and catarrhal 
manifestations continue and lead to anorexia, increase of the cough with 
bronchial secretion, wheezing, and dyspnoea. There is usually a slight 
remission of fever on the second and third days. 

On the fourth day when the general symptoms are at their height, 
and the fever often 103° to 104° F., the characteristic eruption appears, 



248 



INFECTIONS OF UNKNOWN ETIOLOGY 



first on the forehead or cheeks, and spreads, within a very short time, 
over the entire body. The eruption consists of minute purplish-red 
papules, which are slightly elevated, and tend to coalesce to form cres- 
centic figures with intervening areas of clear skin, giving rise to a 
blotched or mottled appearance. Usually confluent, the eruption may 
remain* discrete, especially on the trunk and limbs. In severe cases it 
is quite dusky in appearance and the affected skin is much swollen. 
Being hyperemic, it usually disappears on pressure, but hemorrhages may 
occur. In most cases there is usually swelling of the lymph nodes, 
especially those of the neck. 



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The temperature curve in measles, 



complicated by pneumonia, in a boy, aged five years. 
(Tuley.) 



Preceding the rash by twenty-four, sometimes forty-eight, hours or 
more, the Filatow-Koplik spots, a characteristic feature of the disease, 
may be observed on the buccal and the labial mucous membrane. 
These consist of small, irregular spots of bright red color, in the centre 
of which, in strong daylight, a minute bluish speck may be seen. 

By the fifth day, in the majority of cases, the fever, the general symp- 
toms, and the eruption have reached their height. By the sixth or seventh 
day, after having lasted two or three days, the rash begins to fade as it 
developed, from the face first, and it is succeeded by a branny desquam- 
ation. The nasal discharge lessens, the cough becomes looser, and there 
may be free expectoration. By the eighth day, usually, the temperature, 
having fallen by rapid lysis, is normal and convalescence is established. 






MEASLES 249 

Varieties. — In unusual or atypical cases, the rash may occur unusually 
early, within thirty-six hours, or it may be unduly delayed (sixth day). 
In other cases of house epidemics the child may manifest the initial 
coryza and no eruption at all may appear. Hemorrhagic measles is a 
severe infection, attended by petechial eruption, sometimes hemorrhages 
from the mucous membranes, and marked prostration from toxemia. 
It is often fatal, and occurs usually in institutions or barracks where 
the sanitary arrangements are bad. 

Complications and Sequels. — Capillary bronchitis or bronchopneumonia, 
which is responsible for most of the fatalities, with atelectasis, may 
result from extension of the ordinary bronchitis. The less common 
complications are lobar pneumonia, pleuritis, severe catarrhal pseudo- 
membranous inflammation of the mouth and larynx, oedema of the glottis, 
catarrhal inflammation and suppuration of the middle ear, gastro- 
enteritis, gangrene of the mouth, vulva, etc. Tuberculosis of the lungs 
and of the bronchial and mediastinal lymph nodes is an important and 
not infrequent sequel. Arthritis and paralysis due to myelitis and 
multiple neuritis (polyneuritis) have been observed. 

Diagnosis. — The diagnosis is usually easy. The presence of an epi- 
demic, initial coryza, fever, and catarrh of the respiratory mucous 
membrane, suggest the disease, even before the appearance of the path- 
ognomonic Filatow-Koplik spots and the characteristic eruption. From 
scarlatina measles may be distinguished by the longer preemptive stage, 
the general catarrhal symptoms (instead of mere sore throat), the 
Filatow-Koplik spots, the blotched or mottled appearance of the rash 
with special involvement of the face (as distinguished from the more 
uniform erythema of scarlatina with relative freedom of the face), the 
absence of leukocytosis (except in the event of complications), the 
absence of undue acceleration of the pulse, absence of the characteristic 
scarlatinal tongue, and the fall of temperature after the rash is well out. 

It may be difficult or impossible in some cases to differentiate measles 
from rotheln, but rotheln is suggested by less fever, shorter preemptive 
stage (one or two days), less catarrhal symptoms, more sore throat, 
general uniform distribution of the rash, absence of crescentic arrange- 
ment, and very slight desquamation. The presence of fever and catarrhal 
symptoms serve to differentiate measles from urticaria and multiform 
erythema, as well as from different drug eruptions, in which the history 
also may be of service. The initial eruption of smallpox may be mis- 
taken for measles, but the differential diagnosis does not long remain in 
abeyance. Four days of fever and catarrh usually exclude variola, 
varicella, rotheln, and scarlatina. 

Prognosis. — The prognosis is favorable in simple cases. Complica- 
tions, such as bronchopneumonia, hemorrhagic rash, etc., render the 
prognosis grave. 

Treatment. — Hygienic regulations (page 29), rest in bed, and light 
nutritious diet are most important. Otherwise the treatment is purely 
symptomatic. The fever is rarely high enough to demand special 



250 Infections of unknown etiology 

attention, but the general comfort of the child may be enhanced by daily 
tepid sponging or a tepid bath, especially if the temperature is about 
103° F. Should the rash not appear, a hot bath and warm drinks will 
please the elderly nurse and do no harm: they are believed to hasten 
the development of rash. The distressing cough and the general con- 
dition of the child may be relieved by a mild, sedative and diaphoretic 
fever mixture, such as the following: 

1$ — Spirit of nitrous ether 3 drams 12 00 

Camphorated tincture of opium 2 drams 8 00 

Wine of ipecac 1 dram 4 00 

Solution of ammonium acetate, sufficient to make . . 3 ounces 100; 00 — M. 

S. — To a child, two years old, one teaspoonful (5 c.c.) every three hours. 

During desquamation the skin should be anointed daily with vaseline, 
olive oil, or cacao butter, and the daily bath continued. Great care 
must be exercised during convalescence, especially if the child is weakly. 
Nutritious diet, milk, tonics, such as iron, quinine, and strychnine, 
hypophosphites, and cod-liver oil subserve a useful purpose. 



ROTHELN. 

(Rubella; German Measles; Rubella Notha; Epidemic Roseola.) 

Rotheln is an acute, specific, infectious, and highly contagious disease 
characterized by slight fever, coryza, and a maculopapular rash. 

Etiology. — Rotheln occurs during childhood and in adult life, but it 
is more common during childhood, and attacks the sexes equally. 
Sporadic cases are common, but the disease often appears epidemically. 
One attack usually confers immunity, but recurrences have been observed. 

The exciting cause of the disease has not been isolated, though it 
seems to be present in the emanations from the patient, especially the 
nasal and oral discharges and the skin lesions. The disease is highly 
contagious and spreads with extreme rapidity. Infection may be trans- 
mitted by direct contact, by a third person, and by fomites. Infection 
is acquired by inhalation. The patient is infectious from the period of 
incubation until convalescence. 

Pathology. — There are no characteristic anatomical lesions. 

Symptoms. — The period of incubation is usually from ten to twelve 
days, but it has been reported to vary between three days and three weeks. 
The invasion is usually mild, and may be devoid of prodromal symp- 
toms, although chilliness, mild fever (rarely more than 100° F.), malaise, 
headache, backache, coryza, sore throat, and dry cough may be observed 
for a day or two. Usually on the second day, that is, at the end of the 
first twenty-four hours (sometimes earlier), the characteristic rash ap- 
pears — first on the oral and faucial mucous membrane and the face, 
then on the chest, and within twenty-four hours spreads over the entire 
body. In some cases, however, it remains curiously restricted to certain 



ROTHELN 251 

parts of the body, and may be observed only on the roof of the mouth 
and the fauces. The eruption consists of rosy-red, slightly elevated 
papules, that are usually discrete, though they may become confluent. 
They show little tendency to form crescentic patches, and the intervening 
skin is often hyperemia With or just before the appearance of the rash 
the temperature may become a little more elevated, and it remains 
usually between 100° and 102° F. while the rash is out; the pulse is 
proportionately rapid; coryza, conjunctivitis, sore throat, and evidences 
of bronchitis become more marked ; and the cervical lymph nodes (rarely 
other lymph nodes) are enlarged. The rash lasts usually two to five 
days, gradually fades, and is succeeded by a very slight branny desquama- 
tion and a brownish discoloration of the skin, which disappears after 
a day or two. With the fading of the rash the general symptoms lessen, 
and convalescence is usually established at the end of a week. 

Complications. — Severe bronchitis and bronchopneumonia sometimes 
occur. 

Diagnosis. — Considerable confusion in diagnosis often occurs, inasmuch 
as rotheln exhibits the sore throat of scarlatina and the rash of measles. 
From measles, however, rotheln may be distinguished by the less fever, 
shorter preemptive stage, less catarrhal symptoms, more sore throat, 
general uniform distribution of the rash, absence of crescentic arrange- 
ment, and very slight desquamation. From scarlatina rotheln may be 
distinguished by the less abrupt onset, less high fever, less rapid pulse, 
absence of vomiting, absence of the strawberry tongue, absence of a 
punctiform rash, and the non-occurrence of nephritis. Dukes' so-called 
"fourth disease" is a disorder of which the incubation period is that of 
German measles; prodromes are usually absent; the onset is abrupt, 
with moderate fever, sore throat, and a rash that may cover the body 
within a few hours, although the face may remain free; the rash is 
brighter red than that of scarlatina, and may be followed by slight 
desquamation (more than in rotheln), rarely by marked desquamation; 
there are no sequels; and the disease does not protect against rotheln 
or scarlet fever. Whether or not it is an independent disease has not 
been determined. Infectious erythema is a disorder described by Esch- 
erich, and characterized by a rose-red, maculopapular (morbilliform) 
rash developing especially on the face and the flexor surfaces of the 
extremities; it occurs epidemically in children between the ages of four 
and twelve years; there may be no subjective symptoms; the rash 
usually fades in five to six or ten days, and is not followed by des- 
quamation. 

Prognosis. — Recovery is the rule. 

Treatment. — The treatment is similar to that of measles. 



252 INFECTIONS OF UNKNOWN ETIOLOGY 

GLANDULAR FEVER. 

(Drusenfieber, Pfeiffer.) 

Glandular fever is an acute, infectious, and moderately contagious dis- 
ease, characterized by fever and swelling and tenderness of the lymph 
nodes. 

Etiology. — Glandular fever is essentially a disease of childhood, 
though a few cases have been observed in adults. It often prevails 
epidemically, especially in the late fall, the winter, and the spring, but 
sporadic cases are sometimes observed. A specific exciting cause of the 
disease has not been isolated. Streptococci, staphylococci, influenza 
bacilli, and pneumococci have been found in the oral secretions in 
different cases, and suggest the opinion that the disease is probably not 
always due to the same cause. The disease is contagious, but how 
the contagium is transmitted has not been determined with certainty. 
Infection is believed to be acquired by inhalation, the causative bacteria 
acquiring a nidus in the mouth and the upper respiratory tract, whence 
they readily gain access to the regional lymph nodes. 

Pathology. — The conspicuous feature of the disease is inflammatory 
swelling of the lymph nodes, especially the cervical, but sometimes also 
the axillary, inguinal, and mesenteric. 

Symptoms. — The period of incubation is not definitely known, but 
it is probably several days. The onset is usually abrupt, with chill or 
chilliness, fever (101° to 103° F.), headache, restlessness, sometimes 
nausea and vomiting, and pain in the neck, especially on motion. Some- 
times there is complaint of sore throat, and slight swelling and redness of 
the tonsils may be discovered. Usually on the second day the enlarged 
lymph nodes become apparent — swollen, painful, varying in size from that 
of a pea to a walnut, and not infrequently associated with periglandular 
oedema. Cough and oppression in the chest sometimes suggest involve- 
ment of the bronchial lymph nodes. The mesenteric nodes are some- 
times palpable, and explain the rather common abdominal pain and ten- 
derness. The bowels are usually constipated, and pains in the joints are 
not infrequent. The fever continues, as a rule, about a week and falls 
by lysis; the lymph-node enlargement lasts from two to three weeks, and 
gradually subsides. Suppuration is rare. Cutaneous erythemas, otitis 
media, bronchopneumonia, and nephritis are the more common com- 
plications, and are answerable for the few fatalities. 

Diagnosis. — The diagnosis is usually easy, but occasionally, especially 
in the event of the cutaneous rash, one must be careful to exclude scar- 
latina. 

Treatment. — Rest in bed during the period of fever at least, a liquid 
diet, an antiseptic mouth wash, a preliminary course of calomel, and a 
mild diuretic fever mixture (such as that mentioned on page 250) are all 
that are required — since we are unable directly to influence the duration 
of the disease; but one should endeavor to prevent complications. 



RHEUMATIC FEVER 253 

RHEUMATIC FEVER. 

{Acute and Subacute Rheumatism; Articular Rheumatism.) 

Rheumatic fever is an acute and subacute (possibly specific) infectious 
and non-contagious disease, characterized by fever, multiple arthritis, 
sweating, and a tendency to inflammation of the serous membranes and 
the fibrous tissues of the body. 

Etiology. — Rheumatic fever occurs especially in adults between the 
ages of fifteen and thirty-five years, but no age is exempt, and the disease 
has been observed in very young children. In children, however, 
the arthritic manifestations are often quite subsidiary to the cardiac. 
The disease is especially common in those exposed to the influences of 
wet, cold, and sudden changes in temperature — hence males rather than 
females, and among men, laborers, coachmen, drivers, sailors, etc., 
and among women, serving-maids, washerwomen, etc. Between the 
ages of ten and fifteen years, however, girls are more commonly affected, 
while prior to the tenth year the sexes suffer equally. The disease is 
endemic in temperate climates, and prevails especially during February, 
March, and April, but also during the colder months. Occasionally 
it exhibits epidemic characteristics. One attack, rather than conferring 
immunity, predisposes to subsequent attacks. 

The exciting cause of the disease has not been isolated, although 
etiological importance has been attributed to a number of different 
microorganisms, and the anatomical and clinical characteristics of the 
disease permit of no doubt of its being an infection. Possibly the same 
etiological factor is not operative in all cases, and we may jet be able 
to differentiate a true rheumatic fever from other pseudorheumatic, 
pyemic, or toxic disorders with arthritic manifestations. Although the 
disorder has been attributed to streptococci, staphylococci, etc., the most 
likely causative factor is a diplococcus studied by Poynton and Paine, 
who isolated it from the joint lesions, the rheumatic nodules, the blood, 
etc., and were able to produce arthritis, valvulitis, etc., in rabbits. How 
infection is acquired has not been definitely determined for all cases, but 
there is an increasing disposition to regard the tonsils as the portals of 
entry for the infection in many, if not all, cases: the clinical relation 
is undoubted. 

Pathology. — The inflammatory manifestations in the joints, serous 
membranes, and fibrous tissues exhibit scarcely anything characteristic, 
with the possible exception of the rheumatic nodule (found in tendon 
sheaths and over bony prohiinences), which consists of a central area 
of necrosis, surrounded by swollen and cedematous connective tissue 
and cellular exudation. The articular fluid is turbid, albuminous, and 
usually contains a few fibrin flakes and leukocytes. 

Symptoms. — The period of incubation is not definitely known. Pro- 
dromes, such as malaise, irregular, fugitive pains, and sore throat (ton- 
sillitis) may be present for a few hours or a day or two ; but, as a rule, the 



254 INFECTIONS OF UNKNOWN ETIOLOGY 

disease sets in abruptly with chilliness (occasionally a definite chill), fever, 
and inflammatory manifestations in one or several joints. The affected 
joints are usually the larger joints — the knee, ankle, shoulder, elbow, 
and wrist; less commonly the hip, fingers, toes, and intervertebral joints. 
They are swollen, red, hot, painful, and tender; motion is much restricted 
and when made aggravates the pain. A characteristic of the joint lesions 
is their fugaciousness, the fact that the inflammatory phenomena some- 
times develop and subside with marked rapidity (but sometimes more 
slowly), and that they flit from one joint to another. In different cases, 
therefore, at one time, one or several joints may be involved in varying 
degrees. In some cases, later in the course of the disease, the lesions 
show a disposition to linger in certain joints. It is rare, however, for 
a single joint only to be involved. Intra-articular effusion is usually 
slight or moderate, the marked swelling of the joint being due largely to 
serous infiltration of the periarticular tissues — the tendon and muscular 
sheaths, bursse, etc. Rheumatic nodules (misnamed fibrous nodules) are 
present in some cases, and are of much diagnostic importance. They are 
more common in children than in adults, and consist of small swellings 
(1 to 4 mm. in diameter) attached to bony prominences (the periosteum) 
or tendon sheaths just beneath the skin — the hands, wrists, elbows, 
vertebrae, etc. They are sometimes more apparent to sight than to 
touch, are usually not tender, and sometimes appear and disappear with 
marked rapidity, although they may last for a long time (when they 
really become fibrous nodules). 

The general manifestations of rheumatic fever are usually subsidiary 
to the articular. The fever, as a rule, varies from 102° to 104° F., 
though hyperpyrexia (106° to 108° F.) is occasionally observed in severe 
cases. The fever pursues an irregular course and ends by lysis. The 
pulse is rapid (above 100) and soft; other symptoms of toxemia are 
present, such as loss of appetite, thirst, coated tongue, constipation, 
enlargement of the spleen, and concentrated urine (which is usually 
highly acid and may be albuminous). Profuse acid sweats of a peculiar 
odor are the rule and often correspond with remissions in the tempera- 
ture; and sudamina and milaria are common. Leukocytosis is present; 
a secondary anemia usually develops rapidly. 

Complications. — Complications are many, though doubtless many 
lesions heretofore regarded as complications are really part and parcel 
of the rheumatic fever (manifestations of the rheumatic poison) ; but some 
are the result of secondary infection. Hyperpyrexia (108°, even 110° F.) 
is occasionally observed, especially in primary attacks. It is a serious 
symptom, usually associated with severe nervous manifestations, such as 
delirium, rapid pulse, marked prostration, and frequently soon leads to 
death. The term "cerebral rheumatism" has been given to some 
cases in which toxic (nervous) symptoms are severe, usually from the 
beginning. To the high fever, delirium, and rapid pulse, evidences of 
motor irritability (tonic spasms, sometimes general convulsions) may be 
added; these are often followed by coma and death. The brain at 



RHEUMATIC FEVER 255 

necropsy usually reveals no lesions; in some cases meningitis (purulent 
and other) has been found; but these cases were probably not true 
rheumatic fever, the joint lesions being pyemic and improperly inter- 
preted clinically. Delirium and coma may occur without hyperpyrexia — 
being in some cases uremic. Chorea may occur in association with or as 
a sequel to rheumatic fever. Cardiac complications are the most com- 
mon, and in many respects the most serious. Myocarditis (toxic) is 
common in the early stages and often leads to dilatation. Endocarditis 
occurs in many cases (50 to 75 per cent.), and its likelihood increases 
with the youth of the patient and the number of attacks. The lesions 
most frequently involve the mitral valve, and may be benign (usually) 
or malignant (unusually). Often the lesions are mild and overlooked, 
and are not detected until later in life, when sclerotic changes in the valve 
segments have occurred. Many of the murmurs that develop during 
rheumatic fever, however, are not attributable to endocarditis, but to 
dilatation of the heart or the very common anemia, and they disappear 
with convalescence. Pericarditis is not uncommon, and is found in 
most fatal cases. It may be fibrinous, serofibrinous, or purulent. In 
many cases the lesions constitute a pancarditis. Serous pleuritis and 
even serous peritonitis may also occur, and two or more serous mem- 
branes may be involved simultaneously — a multiple serositis. Con- 
gestion of the lung and pneumonitis are observed in some cases and 
may prove fatal. Tonsillitis and pharyngitis are sometimes marked; 
nephritis is rare. Different skin lesions have been observed — sudamina, 
miliaria (already mentioned), urticaria, multiform erythema, scarlatini- 
f orm rash, purpura, etc. ; so-called purpura (peliosis) rheumatica is really 
not a rheumatic affection. The muscles are often swollen and painful, 
and sometimes become atrophic (arthritic atrophy). 

Rheumatic fever in children usually sets in abruptly with high fever, 
and sometimes convulsions. It involves the joints, as a rule, less than 
the heart — myocarditis (with dilatation), endocarditis, pericarditis; 
anemia and exhaustion develop apace, and if the child does not soon die, 
the fatal termination from valvular disease, etc., is usually merely a 
question of time. Aberrant rheumatism is quite common in children — 
growing pains, stiff neck, recurring tonsillitis, etc. 

Diagnosis. — The diagnosis is usually quite apparent from the fever, 
polyarthritis (and its peculiarities), acid sweats, and the rarity of in- 
/olvement of the temporomaxillary, sternoclavicular, sacro-iliac, intra- 
vertebral, and pubic joints. Gonorrhceal arthritis may be distinguished 
oy a history of gonorrhoea; involvement of one joint often (especially 
the knee or wrist), although several joints may be involved; severity of 
the local lesions — extreme pain and marked swelling due chiefly to peri- 
articular oedema; persistence of the articular lesions — often leading to 
more or less permanent disability of the joint; relative absence of general 
symptoms — little fever, etc. Acute osteomyelitis, involving especially the 
lower end of the femur or the upper end of the tibia, may be distinguished 
by the involvement of the epiphysis and shaft of the bone (rather than the 



256 INFECTIONS OF UNKNOWN ETIOLOGY 

articulating surfaces), the great intensity of the local signs, and the 
grave constitutional symptoms (pyococcic). Acute arthritis, such as may 
occur in infants, in scarlatina, in cerebrospinal meningitis, in puerperal 
infection, etc., is usually septic in character (pyococcic), may go on to 
suppuration, and is attended by the usual symptoms of septicemia — 
chills, fever, sweating, etc., and a focus of infection may often be demon- 
strable. If not pyococcic, the so-called acute rheumatic joints of chil- 
dren are likely to be syphilitic or scorbutic. Gout may be distinguished 
by its occurrence in males (especially beyond the fiftieth year), its char- 
acteristic onset, predilection for the great toe (though other joints are 
often involved), uratic deposits in the body, and an analysis of the urine. 

Prognosis. — Rheumatic fever is very variable in its course, though it 
usually terminates in recovery without permanent damage to the joints 
in from two to six weeks. In some cases, however, recovery is less 
rapid, and exacerbations of fever and articular lesions recur from time to 
time — subacute rheumatic fever. The prognosis is worse in children than 
in adults, and in both is influenced by the occurrence of complications — 
some of which, such as hyperpyrexia and purulent pericarditis, are 
immediately serious, whereas others, such as endocarditis, are of more 
remote concern. One attack predisposes to others. 

Treatment. — The patient should be confined to bed, even in the mild 
cases, and should wear a flannel night gown and sleep between blankets. 
The diet should consist largely of milk, but broths and soups may be 
allowed, and water should be given in large quantities. Salicylic acid 
and its derivatives exert a more or less specific action and should be given 
in full doses at the outset in all cases with the idea of obtaining an 
immediate effect. In a case of average severity in an adult sodium 
or ammonium salicylate, aspirin, salicin, salicylic acid, or other 
well-known salicyl compounds, should be administered in 20 grain 
(1.3 gram) doses, every two hours, until the symptoms abate or 
manifestations of salicyl intoxication supervene. By the third day 
usually the dose may be reduced to 15 grains (1 gram) every four or 
five hours. If symptoms of marked intoxication (tinnitus aurium, gastric 
irritability, delirium in some cases), supervene, the drug may be with- 
drawn for twelve to eighteen hours. Oil of wintergreen in 20 minim 
(1.25 c.c.) doses may be substituted for the other salicyl compounds. 
Should the attack not respond to the salicylates, the so-called alkaline 
treatment may be employed, or both may be used together — a form of 
treatment especially serviceable in children. To an adult 30 grains 
(2 grams) of potassium bicarbonate may be given every two or three 
hours for the first few days or until the urine is alkaline; or potassium 
acetate or citrate or sodium bicarbonate may be used. The salicyl 
treatment seems to relieve the joint symptoms, to shorten the course of 
the disease, to render relapse less likely, and to protect the heart, although 
endocarditis appears to be less common under the alkaline treatment. 
With a view to protect the heart, Caton urges the use of small blisters 



PERTUSSIS 257 

ap ively along the course of the third, fourth, fifth, and 

si: )stal nerves. 

he local articular symptoms is of the utmost importance; 
bu of treatment suggested, none is so valuable as absolute 

ret e beneficent influence of rest enjoined by a splint the 

loc u tenderness often subside almost immediately. In addi- 

tion the joint may be wrapped in cotton wool, or in cloths saturated with 
lead water and laudanum, or a saturated solution of magnesium sul- 
phate; or an ointment of methyl salicylate (20 per cent.) may be applied. 
Occasionally the pain is so severe as to call for the use of morphine, 
especially at night. In this event a Dover's powder is often serviceable. 
The coal tar products are scarcely ever necessary. Hyperpyrexia calls 
for the cold bath or the cold pack. Since anemia usually develops 
rapidly, iron is practically always indicated during convalescence, when 
quinine and strychnine will be found useful adjuvants. 



PERTUSSIS. 

(Whooping Cough.) 

Pertussis is a subacute, specific, infectious, and moderately contagious 
disease, characterized by catarrhal inflammation of the respiratory 
mucous membrane and paroxysms of convulsive coughing that terminate 
in a protracted inspiration — the "whoop." 

Etiology.— Pertussis is essentially a disease of childhood, being espe- 
cially prevalent between the second and the seventh year. It is unusual 
under six months of age. It probably attacks the sexes equally, although 
girls are said to be more susceptible than boys. It sometimes occurs 
in non-immune adults, and even in elderly persons, in whom it usually 
runs a severe and frequently fatal course. In some cities the disease is 
endemic ; in most sections of the country sporadic cases occur from time 
to time ; but the disease usually prevails epidemically in the winter and 
spring. It frequently follows or precedes epidemics of measles, rarely epi- 
demics of scarlatina. One attack usually establishes immunity, although 
recurrences are observed. Some persons possess a natural immunity. 

The exciting cause of the disease is probably a bacillus, somewhat 
resembling the influenza bacillus, found by Koplik, and by Czaplewski 
and Hensel, in the mucous discharges. The disease is only moderately 
contagious, and especially during the catarrhal stage. Infection is 
usually transmitted directly, but it may be transmitted by a third person 
and perhaps by fomites. It is acquired through inhalation, and is some- 
what favored by overcrowding, such as obtains in close, insanitary 
dwellings, school rooms, etc., and by previous ill health, especially catarrh 
of the air passages; but prolonged personal contact with an infected 
person seems necessary for infection. 

Pathology. — Pertussis is devoid of characteristic lesions. The lesions 
found after death are those of the complications, such as broncho- 
17 



258 INFECTIONS OF UNKNOWN ETIOLOGY 

pneumonia, capillary bronchitis, atelectasis, emphysema, etc., but they 
present nothing characteristic. 

Symptoms. — The period of incubation is from seven to ten days. 
Clinically the disease may be divided into two stages — the catarrhal and 
the paroxysmal. The invasion is rather slow, the disease beginning 
as an ordinary catarrh of the air passages, with injection of the conjunc- 
tivae, coryza, cough, a few rales, and moderate fever (102° R). Grad- 
ually the paroxysmal stage is developed. At the end of ten or fourteen 
days, the fever having almost if not entirely subsided, the cough, instead 
of improving (as in ordinary catarrh), gradually becomes extremely 
severe and paroxysmal in character, in some cases especially at night. 
A typical paroxysm consists of a series of short coughs, increasing in 
severity and interrupted only occasionally by a prolonged inspiration — 
the characteristic whoop. The child begins to cough, the expiratory 
efforts succeed one another with great rapidity until the lungs are almost 
emptied of air (sometimes they last even longer, consisting then of 
purposeless and almost noiseless vibrations of the chest wall), until 
finally with apparently a great effort a prolonged high-pitched crowing 
inspiration— the " whoop" — follows through the partially closed glottis. 
During the attack the child becomes more or less asphyxiated — the face 
becomes swollen and livid, the cervical veins swell, the conjunctivae 
become injected, the eyes protrude and become bathed in profuse 
lacrymation, and subconjunctival and subdermal facial ecchymoses, 
and even hemorrhages from the nose, mouth, and sometimes the 
lungs, may occur. Usually the attack is terminated by the expectora- 
tion of a small amount of characteristic, tenacious, glairy mucus; fre- 
quently the attack terminates in vomiting, which serves to eject a con- 
siderable amount of tenacious mucus. The paroxysms may occur singly 
or several may follow in rapid succession, and they may be repeated 
several times or as often as forty or fifty times during the twenty-four 
hours. During the intervals, in the absence of complications, such as 
bronchopneumonia, the child may appear relatively well and may play. 
Spells of coughing devoid of the terror and not followed by the typical 
whooping spells may also occur. In adults the paroxysms are usually 
less severe and less typical than in children. A lymphocytic leukocy- 
tosis is present in about 85 per cent, of the cases, especially during 
the early (catarrhal) stage. The physical signs are those of bronchitis, 
and are not distinctive. 

Having lasted three or four weeks, as a rule, the paroxysms gradually 
lessen in severity and frequency, expectoration becomes freer, muco- 
purulent in character, and gradually lessens (the stage of decline). The 
paroxysms, however, may last for weeks, even months, and emotion and 
excitement have been known to provoke an attack long after the disease 
has been apparently cured. 

Complications and Sequels. — The most frequent and most important 
complication is bronchopneumonia, or capillary bronchitis, which is 
responsible for most of the fatalities. Emphysema sometimes arises in 



PERTUSSIS 259 

consequence of the severe coughing. Usually it subsides, but it may form 
the basis of an emphysema that may give rise to symptoms in later life. 
Hemorrhage into the brain, occasioning convulsions, paralysis, even 
death, has occurred. Anemia and marked emaciation sometimes result 
from defective nourishment occasioned by the repeated vomiting. 
Ulceration of the frenum of the tongue sometimes results from forcible 
projection of the tongue against the teeth. Severe heart strain and its 
consequences, tuberculosis, swelling of the bronchial lymph nodes (suffi- 
cient to occasion substernal and vertebral dulness), nephritis, temporary 
glycosuria, noma, etc., have been observed as sequels. 

Diagnosis. — The diagnosis in the early or catarrhal stage is impossible. 
As soon as the whoop appears the diagnosis is clear. In the absence of 
an epidemic, however, the disease may be suspected in the event of severe 
coughing (without the whoop) and vomiting, puffiness of the con- 
junctiva, or swelling and duskiness of the face. 

Prognosis. — In consequence of the common association of complica- 
tions, pertussis is a very fatal disease — the mortality in some epidemics 
being as high as 12 per cent. It is especially fatal in children under 
two years of age, and in the weakly. 

Treatment. — The patient should be isolated and the ordinary measures 
of prophylaxis carried out (page 29) . During the catarrhal stage rest in bed 
is essential, and the room should be well ventilated by day and by night. 
If two rooms are available, the child may be taken from one to the other, 
and each fumigated daily with a view to prevent re-infection. The diet 
should consist largely of milk, but after the catarrhal stage has passed 
other articles of a readily assimilable nature may be permitted — bearing 
in mind the frequent vomiting induced by the paroxysms of coughing. 
Sometimes it is wise to give a small amount of food immediately after the 
cessation of a paroxysm that has brought on vomiting. During the 
catarrhal stage a simple febrifuge or sedative expectorant mixture, such 
as is serviceable in an ordinary acute bronchitis, may prove of value. 
For treatment during the paroxysmal stage many remedies have been 
suggested from time to time, but none is really satisfactory. Quinine 
has long been used, and is probably as satisfactory as any drug — J grain 
(0.01 gram) for each month of age, or 1.5 grain (0.09 gram) for each year 
of age under five years, three times daily. Jacobi has obtained the best 
results from the use of belladonna when given to the physiological limit. 
Many writers extol the virtues of antipyrin, 1 grain (0.06 gram) three times 
daily to a child of one year. Its ill effects may be somewhat neutralized 
by the concurrent use of whiskey; and it may be combined with the 
bromides or with belladonna; or belladonna may be combined with the 
bromides. Bromoform, asafcetida, and many other remedies have 
enjoyed a more or less ephemeral reputation. Local treatment is some- 
times efficacious — sprays or swabs to the throat of hydrogen peroxide, 
resorcin (1 per cent.), and other antiseptics; or compound tincture of 
benzoin, creosote, carbolic acid, or oil of eucalyptus, by inhalation (croup 
kettle). Spirit of chloroform, or chloral, or rarely opium (paregoric, 



260 INFECTIONS OF UNKNOWN ETIOLOGY 

Dover's powder, heroin, or morphine) may be resorted to in severe cases 
at night to insure rest. An elastic binder, as originally recommended by 
Kilmer, is of service in obviating vomiting, as well as in supporting the 
abdominal wall during severe paroxysms of coughing. 



INFECTIOUS PAROTITIS. 

(Epidemic Parotitis; Mumps.) 

Infectious parotitis is an acute, infectious, and moderately contagious 
disease, characterized by inflammation of the parotid gland, and exhibit- 
ing a predilection to involve the testicles, the breasts, and the ovaries. 

Etiology. — Infectious parotitis is most common in children, but it 
occurs also in adults; it is rare in infants and the aged. It is more com- 
mon in males than in females. It usually prevails epidemically, espe- 
cially in the late fall, the winter, and the early spring, but sporadic cases 
are not uncommon. The exciting cause of the disease has not been 
isolated. The disease is contagious, and though the contagium may be 
transmitted by fomites, rather close personal contact seems necessary 
for infection in most cases. The breath and the saliva are believed 
to be infectious — for about three weeks. Infection is probably acquired 
by inhalation and is transmitted along Stenson's duct. 

Pathology.— The lesions consist of swelling of the mucosa of Stenson's 
duct, and hyperemia and oedema (sometimes minor inflammatory altera- 
tions) of the parotid gland and the periglandular tissues. 

Symptoms. — The period of incubation varies from one to three weeks, 
and, as a rule, is unattended by prodromal symptoms. The onset is 
usually with moderate fever (101° to 102°, occasionally 103° to 104° F.), 
pain at the angle of the jaw, headache, and general malaise. Swelling 
of the parotid begins soon, and at the end of thirty-six or forty-eight 
hours is usually quite marked — occasioning swelling in front of and 
below the ear and elevating the ear. Sometimes the swelling and 
oedema extend far onto the cheek, into the infraparotid region, and the 
floor of the mouth. The region is painful (though rarely as painful as one 
might judge from the extreme swelling) and tender; opening the mouth, 
chewing, and swallowing cause distress; and usually there is ptyalism 
(though occasionally the mouth is very dry). In most cases the lesions 
are unilateral at first (most frequently left-sided), but in a day or two 
both glands are usually involved. Occasionally the other salivary 
glands are swollen; the spleen is usually enlarged and may be 
palpable. In a few cases there is quite high fever and marked prostra- 
tion. The fever subsides by lysis, and by the seventh to tenth day 
the patient is usually convalescent. Suppuration is quite rare, and a 
second attack is uncommon (though not unknown). 

Complications. — Orchitis is common after puberty, and may be 
single or bilateral. It usually develops as the parotid swelling subsides; 
rarely it precedes the parotitis. Atrophy not infrequently ensues in 






YELLOW FEVER 261 

severe cases. Vulvovaginitis is not uncommon in young girls; the 
breasts may become enlarged and painful; and rarely the ovaries are 
swollen and tender. Rarer complications comprise otitis media, menin- 
gitis, and divers nervous disorders (paralyses, etc.). 

Diagnosis. — The diagnosis is usually easy. One should exclude 
disorders of the throat that might cause enlarged lymphatics, as well as 
dental caries with suppuration, etc. 

Prognosis. — The prognosis is good; suppuration is rare, and a second 
attack uncommon. 

Treatment. — Rest in bed is advisable. The bowels should be well 
opened with a saline cathartic. A simple diuretic fever mixture (aconite, 
potassium, citrate, etc.) is serviceable in many cases. An antiseptic mouth 
wash, hot fomentations, an ice-bag, or ichthyol ointment may be applied 
to the parotid swelling. In the event of high fever and delirium, the 
usual hydropathic and other treatment for such toxemic states is called 
for. Should orchitis develop, the patient must be put absolutely at 
rest, the testicles elevated, and lead water and laudanum, or some similar 
preparation, applied. 

YELLOW FEVER. 

Yellow fever is an acute, specific, infectious disease, characterized 
by fever, jaundice, albuminuria, and a disposition to hemorrhage, 
especially from the gastric mucous membrane. 

Etiology. — Yellow fever is endemic in the West Indies and Central 
American sea ports ; Havana was for more than a century a well-recog- 
nized focus of endemic infection, whence the disease was periodically 
widely disseminated. The spread of the disease is favored by general 
insanitary conditions, low lands, and the summer months — all of which 
are now known to bear an intimate relation to the mosquito. One 
attack confers immunity. The apparent immunity of natives in yellow 
fever zones is due largely to their having survived an attack of the 
disease during childhood. 

Though Carlos Finlay, in 1881, stated that the mosquito is active in 
propagating yellow fever, the exact etiological factors remained un- 
known until the United States Army Commission, composed originally 
of Drs. Walter Reed, James Carroll, Jesse W. Lazear, and Aristides 
Agramonte, proved the correctness of Finlay's contention, and added 
much additional information — one of the members, Lazear, lost his 
life in the investigation; Reed and Carroll escaped a similar fate, 
but undermined their vitality, and later succumbed. The conclusions 
of the Commission are as follows : (1) The mosquito, Stegomyia fasci- 
ata, serves as the intermediate host for the parasite of yellow fever. 
(2) Yellow fever is transmitted to the non-immune individual by means 
of the bite of the mosquito that has previously fed on the blood of those 
sick with this disease. (3) An interval of about twelve days or more 
after contamination appears to be necessary before the mosquito is 



262 INFECTIONS OF UNKNOWN ETIOLOGY 

capable of conveying the infection. (4) The bite of the mosquito at ail 
earlier period after contamination does not appear to confer any immunity 
against a subsequent attack. (5) Yellow fever can also be experi- 
mentally produced by the subcutaneous injection of blood taken from the 
general circulation during the first and second days of this disease. 
(6) An attack of yellow fever, produced by the bite of the mosquito, 
confers immunity against a subsequent attack of the non-experimental 
form of this disease. (7) The period of incubation in thirteen cases 
of experimental yellow fever has varied from forty-one hours to five 
days and seventeen hours. (8) Yellow fever is not conveyed by fomites, 
and hence disinfection of clothing, bedding, or merchandise, supposedly 
contaminated by contact with those sick with this disease, is unnecessary. 
(9) A house may be said to be infected with yellow fever only when there 
are present within its walls contaminated mosquitoes capable of con- 
veying the parasite of this disease. (10) The spread of yellow fever 
can be most effectually controlled by measures directed to the destruc- 
tion of mosquitoes, and the protection of the sick against the bites of 
these insects. (11) While the mode of propagation of yellow fever has 
now been definitely determined, the specific cause of this disease remains 
to be discovered. 

Stegomyia fasciata bites in the day time (which is quite characteristic) ; 
it is a very black mosquito with silver bands on its body and legs, a lyre- 
shaped silver mark on the back being characteristic. Although the 
specific microorganism of yellow fever has not yet been discovered, it 
passes through a fine porcelain filter, and doubtless therefore belongs to 
the ultramicroscopic organisms. 

Pathology. — Jaundice is constant. The blood is disorganized, and 
hemoglobinemia may be present. Hemorrhages from the mucous mem- 
branes, especially the stomach, are quite characteristic; less frequently 
there are cutaneous and serous membrane hemorrhages. The liver, at 
first, is congested; later it is pale, and reveals fatty degeneration and 
focal necroses. The kidneys and the heart show parenchymatous de- 
generation. The lymph nodes are usually enlarged. 

Symptoms. — The period of incubation is usually two to three days 
(forty-one hours to five days and seventeen hours, according to the United 
States Army Commission), and is usually unattended by prodromes, 
except perhaps slight headache and malaise. The onset of the disease 
is usually abrupt, with chill or chilliness, fever (103° to 104° F.), 
headache, severe pains in the eyes, the back, and the legs, epigastric 
distress, nausea, vomiting, coated tongue, and constipation. On the 
first day often a peculiar facies (one of the characteristic symptoms of 
the disease, according to Guiteras) develops — congested face, injected 
eyes, slight swelling of the eyelids and lips, and a noticeable element of 
jaundice (" undoubtedly the most characteristic feature of the facies," 
Guiteras). By the evening of the first day the temperature may reach 
106° F. or more, but in the majority of cases it is scarcely more than 104° 
F.; it remains at this level with slight fluctuations for two or three days 



YELLOW FEVER 263 

and then gradually falls. In very mild cases die lysis may occur even on 
the second day. At the onset the pulse rate is somewhat increased, but 
it is rarely more than 100 or 110; on the second day it begins to fall, 
even with a rising temperature (a second characteristic symptom of the 
disease, Guiteras), and it may be not more than 75, with a temperature 
of 104° F. or more. The pulse becomes still slower during convales- 
cence — 60, 40, even less. Albuminuria is a third characteristic symp- 
tom, according to Guiteras; it varies much in intensity, but is usually 
more marked in the evening urine. In severe cases it may be present 
on the evening of the first day, and it is practically always present by 
the evening of the second day, being one of the few diseases in which 
albuminuria is present very early. It may be slight and transient, but is 
sometimes extreme and associated with tube casts and other manifesta- 
tions of nephritis, and is usually disproportionate to the severity of the 
other symptoms. Complete suppression of urine may supervene and the 
patient may die of uremia even within thirty-six hours. 

With the fall of the temperature, on the third day of the disease, 
the period of remission (so-called period of calm) develops; but this is 
often missed. In favorable cases the patient may now go on to complete 
recovery. Usually, however, he exhibits evidences of infection, such as 
jaundice, epigastric distress, albuminuria, mental dulness, and prostra- 
tion, and at the end of twenty-four or thirty-six hours of comparative 
comfort (in severe cases, without such period) the period of secondary 
fever or collapse supervenes. The fever returns and becomes remittent; 
jaundice and albuminuria increase, and the urine may become almost 
if not quite suppressed; epigastric distress becomes worse; nausea and 
vomiting return, the vomitus consisting at first of the stomach contents, 
but soon of altered blood (black vomit); hemorrhages from the other 
mucous membranes and into the skin may develop ; prostration becomes 
extreme, and the patient passes into a typhoid state (Hippocratic facies, 
coma, delirium, subsultus tendinum, etc.), and commonly dies. Re- 
covery, however, may ensue even in the severest infections. In some 
cases the temperature does not become elevated, but may become even 
subnormal, "black vomit" occurs, the patient collapses, and dies (algid 
form). Mental alertness is a noteworthy feature of many cases, even 
in the presence of "black vomit," but delirium may occur at any time, 
even at the onset; when it occurs later, however, it is due quite as often 
to uremia as to the yellow fever intoxication. The bowels are usually 
constipated, and the stools are bile-stained (normal), but later they may 
contain blood. 

Varieties. — Mild, severe, and fulminant cases may be distinguished. 
The mild cases often escape recognition, since the patient complains only 
of slight indisposition for a day or two, and does not take to bed. In 
certain (fulminant) cases the patient is overwhelmed with the intoxica- 
tion; vomiting, collapse, coma, perhaps convulsions, develop, and the 
the patient dies within a day or two. Convalescence is often protracted, 
and attended with anemia, enteritis, abscesses, parotitis, etc. 



264 INFECTIONS OF UNKNOWN ETIOLOGY 

Diagnosis. — The recognition of the disease is comparatively easy 
during the prevalence of an epidemic, but some epidemics have been so 
mild that much acrimonious discussion regarding their true nature, 
whether the disease is dengue or yellow fever, has arisen, especially in 
the South. In case of doubt, the three characteristic features of the 
disease mentioned by Guiteras should be of much importance. Guiteras 
also believes that a high hemoglobin value (90 to 100 or more) in the 
first four or five days of the disease is of diagnostic value — serving to 
exclude malaria, typhoid fever, and influenza, in which the hemoglobin 
is said to become low early in the disease. In dengue jaundice is not 
so common as in yellow fever, nor does it occur so early, and hemor- 
rhages are less frequent. Pernicious malaria fever may be excluded by 
the absence of malarial parasites from the blood, absence of enlarged 
spleen, and the presence of the characteristic symptoms of yellow fever. 

Prognosis. — The mortality varies in different epidemics between 
15 and 85 per cent., and is in direct ratio to the severity of the infection 
and the resistance of the individual. 

Treatment. — The patient should be quarantined (page 29), and, in 
accordance with what we now know of the etiology of the disease, especial 
attention should be directed to screening the patient's bed, room, or 
house (so as to prevent the access of mosquitoes), and to destroying all 
mosquitoes and their breeding places or places suitable for breeding. 
Special attention must be directed to the occurrence of mild cases, 
especially among children and young adults; these often act as sources 
of infection. 

Since we have no specific, the treatment of the developed disease is 
largely supportive and symptomatic. The patient must rest in bed 
until he is entirely convalescent, and should have a plentiful supply of 
fresh air, sunshine, and light, nutritious food. Hot fomentations to the 
back and epigastrium, and an ice-bag to the head may relieve the pains ; 
morphine and the coal-tar products should be given only in the very 
early stages of the disease, if at all, and very cautiously. Fever calls for 
hydropathic measures — which not only reduce the temperature, but act 
as a general nervous stimulant. Vomiting is often intractable, but may 
be controlled by cracked ice, sips of very hot water, cocaine, or dilute 
hydrocyanic acid. Large amounts of water should be given by the mouth 
(if retained), and saline solutions by the bowels or hypodermicly. Alka- 
lies, such as sodium bicarbonate, may be added to the drinking water, 
to reduce the acidity of the gastric juice (as well as the urine) ; or one 
may use, as advised by Sternberg years ago, sodium bicarbonate, 4 grains 
(0.25 gram), mercuric bichloride, T F5 g Tam (0.0005 gram), and water, 
2 teaspoonfuls (10 c.c.) every hour in a severe case. Other intestinal 
antiseptics may be tried, such as salol, naphthalene, etc. Quinine, as 
well as iron, has been highly recommended, especially to control the 
hemorrhages, over which, however, we can exert very little influence. 
Stimulants are usually called for, sooner or later — strychnine, alcohol, 
etc. Uremia is to be treated on general principles. 



DENGUE 265 

DENGUE. 

{Break-bone Fever; Dandy Fever.) 

Dengue is an acute, specific, infectious, and highly contagious disease, 
characterized by high fever, severe neuromuscular and arthritic pains, 
and an initial erythematous and a subsequent polymorphous rash. 

Etiology. — Dengue prevails endemically, even pandemically, in warm 
climates, such as India, Cairo (and the surrounding country), Java, 
the West Indies, our own Southern States, etc., and during the summer 
months sometimes spreads to the subtropical and temperate zones. 
The disease is highly infectious, and once developed attacks almost 
the entire population almost simultaneously — no age, sex, nor race 
escaping. One attack does not confer immunity. 

The exciting cause of the disease has not been isolated with certainty; 
it is probably ultramicroscopic. Graham, in Beirut, Syria, found what 
he believes to be a hematozoon in the blood, and believes the mosquito, 
Culex fastigans, to be the active factor in propagating it. Ashburn and 
Craig also inculpate the mosquito. 

Pathology. — Since the disease is rarely fatal, careful and extended 
pathological studies have not been carried out. 

Symptoms. — The period of incubation is from one to five days, and is 
unattended by prodromal symptoms. The onset is sudden, with chill 
or chilliness, fever (104° to 107° F.), and severe, even excruciating, pains 
in the head, eyeballs, back, and the extremities (the muscles and joints) — 
whence the term break-bone fever. The large or small joints, and few 
or many, may be affected simultaneously or successively, and in addition 
to being painful, they may be also red and swollen. Furthermore, the 
pulse is rapid, the appetite lost, the urine concentrated, and the patient 
may be slightly delirious; the face is bloated, the eyes injected, and the 
skin and the visible mucous membranes may exhibit a diffuse erythema- 
tous rash, and the skin may be unduly sensitive. On the third or the 
fourth day the fever falls usually by crisis attended by sweating, some- 
times by lysis, and, aside from some muscular soreness and stiffness, the 
patient feels comparatively well. At the end of two or three days of 
apyrexia, the fever and the neuromuscular pains return, but they are 
usually less severe and last not more than twenty-four to forty-eight 
hours; they are often accompanied by a polymorphous rash — measly, 
scarlatiniform, papular, sometimes urticarial and even vesicular — which 
develops first upon the hands, and then spreads to the arms, face/ trunk, 
and legs. This gradually fades and is followed by a fine, branny, often 
almost imperceptible, desquamation. The lymph nodes are often en- 
larged, and may remain palpable well into convalescence or beyond. 
Hemorrhages from the mucous membranes have occasionally been 
observed. 

The disease lasts usually from seven to ten days, but convalescence 



266 INFECTIONS OF UNKNOWN ETIOLOGY 

is sometimes protracted by prostration, anemia, insomnia, even menin- 
gitis, or a relapse. 

Diagnosis. — The epidemic prevalence of the disease, the almost simul- 
taneous implication of a very large portion of the population, the charac- 
teristic fever curve, and the cutaneous rashes serve to distinguish the 
disease, although some difficulty may be experienced in differentiating 
rheumatism in early cases, and influenza, measles, and scarlatina may 
have to be taken into consideration in other cases. Greatest difficulty 
has been experienced in differentiating yellow fever, but yellow fever is 
suggested by the characteristic jaundiced facies, the slowing of the pulse 
with increasing temperature, the early albuminuria, and by the fact that 
slight jaundice, though it may be observed occasionally in dengue, does 
not occur as early as in yellow fever, and hemorrhages are much less 
common. 

Prognosis. — The prognosis is good. Death rarely results, and then 
only in the debilitated, and in the event of coma or hemorrhages. 

Treatment. — The treatment is purely symptomatic. The severe pains 
usually necessitate the use of morphine, although quinine, salol, and other 
salicylates have proved of some service. Tincture of gelsemium has been 
highly recommended by McLaughlin. Chloral and the bromides are 
useful for the insomnia and general restlessness. High fever calls for 
the use of hydrotherapy. Tonics are required during convalescence, 
and potassium iodide is said to be valuable for the persistent arthritic 
pains. 

HYDROPHOBIA. 

(Rabies; Lyssa.) 

Hydrophobia is an acute, specific, infectious disease communicable 
to man by the bite of an animal infected with rabies. 

Etiology. — Rabies is a disease of dogs especially, but occurs also in 
wolves, foxes, cats, rarely in cows and horses, and may be communicated 
to pigs, rabbits, etc. The disease occurs in all parts of the world, 
and is probably more common in spring than in summer (contrary to 
the vulgar opinion). The etiological factor has not yet been isolated, but 
it exists in the saliva, in the brain, spinal cord, and nerves, and probably 
in other secretions, and the blood; it seems not to be present in the 
viscera. It is filtrable and doubtless belongs to the class of ultra- 
microscopic organisms. Infection is transmitted to men usually through 
the bite of a rabid dog, but not more than 10 per cent, of those bitten 
become infected. Children are more commonly affected, because they 
are more frequently bitten. Punctured wounds of the exposed surfaces, 
hands, face, neck, etc., are especially dangerous, clothes largely pre- 
venting wounds of other parts of the body from becoming infected. 

Pathology. — The lesions consist of congestion of the medulla and the 
spinal cord, sometimes associated with minute hemorrhages, and are in 
no way specific — occurring in other convulsive states. Accumulations of 



HYDROPHOBIA 267 

leukocytes about the bloodvessels and nerve cells, especially the motor 
cells of the medulla (Babes' rabic tubercle), are usually present. 
Van Gehuchten and Nelis have described proliferation of the endo- 
thelial cells of the capsules of the intervertebral, pneumogastric, and 
sympathetic ganglia, with destruction of the proper nerve cells. Negri 
has described protozoan-like bodies in the nerve cells, especially those in 
the horn of Ammon, in rabid animals. These lesions may be reproduced 
experimentally and are resorted to for diagnostic purposes. 

Symptoms in the Dog. — Two forms of rabies are recognized: (1) 
Maniacal rabies, in which there is usually a preliminary stage of depres- 
sion, followed by a stage of excitement or mania, in which the dog eats 
little, runs about with saliva drooling, and shows a disposition to bite 
persons, and real and imaginary objects; followed by a third or paralytic 
stage, in which weakness and emaciation proceed rapidly. Death ensues 
usually within eight days. (2) Dumb rabies, in which the second or 
excited stage is absent, and in which paralysis and death occur earlier. 
It is quite important to recognize this form, as, though more readily 
overlooked, it is quite as infectious as the maniacal form, and is the 
only form that occurs in rodents. 

Symptoms in Man. — In man the period of incubation varies between 
two weeks and eighteen months; in most cases it is about eight weeks; 
and in children it is less than in adults. As a rule, the wound heals 
without noteworthy manifestations. The onset of the disease is insidious. 
Toward the end of the period of incubation the site of the wound may 
itch or pain a little, and the adjacent lymph nodes may be somewhat 
enlarged and tender, but often there are no local manifestations. The 
premonitory symptoms, which last one or two days, are depressive — 
melancholia, undue anxiety, loss of appetite; later, perhaps headache, 
irritability of temper, and intolerance for noises, and sleeplessness. 
The temperature may be slightly elevated and the pulse somewhat 
increased in frequency. Gradually spasm of the muscles of deglutition 
and of respiration, and a disposition to refuse water (hydrophobia) is 
developed. The stage of excitement then comes on apace. The spasm 
of the muscles of deglutition and of respiration become more marked; 
they become convulsive in character, and may even spread to the trunk 
and the extremities. They may be excited by the slightest touch, sound, 
visual impression, or auditory suggestion; and the paroxysms induced 
by the sight of water or the attempt to swallow are merely one expression 
of the universal hyperesthesia, of which the greatly exaggerated reflexes 
are another. The paroxsyms, however induced, may last for a few 
minutes or a half hour; they are associated with inability to swallow, 
sensations of extreme dyspnoea (even in the absence of obstruction to 
the air passages), and with the greatest mental anxiety, distress, and 
terror. Thirst is sometimes present, and the temperature is increased 
during the paroxysms. The inability to swallow the saliva (which is 
not infrequently increased), a slight spasmodic cough (designed to 
expel the saliva), and certain guttural sounds produced by spasmodic 



268 INFECTIONS OF UNKNOWN ETIOLOGY 

movements of the larynx, occasion the "frothing at the mouth" and 
the "barks like a dog" associated in the public mind with the disease. 
Between the paroxysms the patient is mentally alert, and only too 
vividly apprehends his danger. Should the patient not die from asphyxia 
or exhaustion, in from two to four days the final, or paralytic, stage sets 
in; the spasmodic attacks lessen and finally cease, the heart becomes 
weak, exhaustion and coma supervene, and in from twelve to twenty- 
four hours the patient dies. 

Diagnosis.— Under no circumstances should the suspected animal be 
killed, except by a physician with a view to secure the nervous tissues, 
examine them, and inoculate them into rabbits — which should always be 
done in animals suspected of rabies. In the event of rabies the inocu- 
lated rabbit dies of the paralytic form of the disease in from fifteen to 
twenty days; whereupon the lesions described by Van Gehuchten and 
Nelis may be found in the plexiform ganglion of the pneumogastric nerve, 
and the Negri bodies may be found in the horn of Ammon. Hydro- 
phobia rather than tetanus is suggested by the history of a bite, the special 
involvement of the muscles of deglutition and of respiration, the psychic 
symptoms, and the absence of lockjaw, of opisthotonos, and of persistent 
tetanic spasm. Pseudohydrophobia or lyssaphobia is a neurosis that 
sometimes develops in hysterical and neurotic subjects, not infrequently 
as early as twenty-four hours after a bite by a rabid or a supposedly 
rabid dog, and often simulates true hydrophobia; usually, however, 
the patient has exhibited considerable dread lest hydrophobia develop, 
and the hysterical element is always in the foreground; the premonitory 
symptoms are missed, there is no true respiratory spasm, obvious imita- 
tions of a dog (such as bites, growls, etc.) are conspicuous, the disorder 
lasts longer than true hydrophobia, and is quite amenable to certain 
severe and well-recognized measures used to control hysterical attacks. 

Prognosis. — No patient has been known to recover from an indubitable 
attack of hydrophobia. 

Treatment.— If possible the wound should be excised; at least it should 
be well laid open and cauterized with nitric acid, carbolic acid, or caustic 
potash, and subsequently treated antiseptically as an open wound (not 
allowed to heal) for several weeks. Pasteur's preventive inoculations 
should be instituted as soon as possible. Pasteur found that the virulence 
of the rabic virus could be markedly increased by passing it through a 
series of rabbits (subdural injections of emulsions of the dog's spinal 
cord) , so that ultimately the period of incubation is reduced to about six 
days, and the duration of the disease to between two and five days. The 
spinal cords of these rabbits contains his virus fixe, which, however, 
gradually loses its virulence upon being dried in the air, and gradually 
becomes inert. Beginning then, with the inoculations of least active 
virus and progressing to those of high activity, immunity in man is 
established (within about two weeks) before the period of incubation 
of the disease occasioned by the dog's bite has elapsed. By this mode 
of treatment, the mortality of an otherwise absolutely fatal disease has 






ROCKY MOUNTAIN SPOTTED FEVER 269 

been reduced almost to a minimum. Aside from the foregoing, treatment' 
is merely palliative. When the disease has developed, the patient should 
be confined to a darkened room, free from noises ; he should be nourished 
by the rectum, and his distress mitigated by chloroform, chloral, mor- 
phine, and the bromides. One may try the Buisson treatment, con- 
sisting of vapor baths and jaborandi, to induce profuse sweating; but 
the treatment has not commended itself to the thinking profession. An 
efficacious antirabic serum has not yet been produced, nor are Pasteur's 
preventive inoculations of the slightest service after the disease has 
developed. 

ROCKY MOUNTAIN SPOTTED FEVER. 

(Tick Fever.) 

Rocky Mountain spotted fever is an acute, infectious disease, occur- 
ring in Western Montana, chiefly in the Bitter Root Valley, as well as 
in Idaho, Wyoming, and Nevada, and characterized by chills, fever, 
neuromuscular pains, and a peculiar maculopapular or petechial eruption. 

Etiology. — Rocky Mountain spotted fever is transmitted by the bite of 
a tick, Dermacentor venustus (andersoni) in Montana, and by Dermacen- 
tor modestus in Idaho ; and is transmissible to the monkey and the guinea- 
pig. The nature of the infectious agent is not known. Wilson and 
Chowning described a small parasite (resembling hyaline malarial bodies) 
which they found in the erythrocytes as well as free in the blood plasma, 
and which they have named Pyroplasma hominis (whence the name for 
the fever, Pyroplasmosis hominis). Stiles and Craig, however, doubt 
the identity of these supposed parasites, Craig stating that the appear- 
ances are due to changes in the hemoglobin. Ricketts has described a 
bacillus found in the tick and their fresh eggs. 

Symptoms. — The period of incubation is said to be from three to 
twelve days. The onset is rather sudden, with chills, headache, nausea, 
neuromuscular pains, and fever. Epistaxis is common, the bowels are 
usually constipated, and there are manifestations of catarrhal inflam- 
mation of the conjunctiva and the upper respiratory tract. The pulse 
is usually disproportionately rapid — 120 to 140. On the second to the 
seventh day of the disease a rather profuse maculopapular (occasionally 
petechial) rash appears. It is usually most marked on the wrists, arms, 
legs, forehead, and later on the trunk. Albuminuria is present in all 
cases. The fever reaches its height (103° to 105° F.) on about the 
twelfth day, and then falls by lysis to reach the normal in four or five 
days or a week. Concurrent with the fall in temperature the rash fades, 
and is sometimes followed by desquamation. Gangrene of the fingers, 
toes, and scrotum has been observed. 

Diagnosis. — The disease is readily recognized in the section where 
it abounds, a history of a tick bite being important. From purpura the 
affection is distinguished by the absence of joint symptoms and of sore 
throat, and the early appearance of the rash, especially on the wrist 



270 INFECTIONS OF UNKNOWN ETIOLOGY 

(as contrasted with its later appearance, especially on the trunk in pur- 
pura). 

Prognosis. — The mortality is very high in some regions — from 70 to 90 
per cent., death occurring usually on about the tenth day; in Idaho it is 
low — 2 to 5 per cent. 

Treatment. — Quinine seems to exert a more or less specific action, and 
should be given in large doses (15 grains, 1 gram, hypodermicly, 
every six hours, Anderson) throughout the course of the disease. Other- 
wise, the disease should be treated as typhoid fever. Stimulants are 
usually called for. 

EPIDEMIC POLIOMYELITIS. 

(Acute Poliomyelitis; Infantile Paralysis.) 

Epidemic poliomyelitis is an acute, infectious, and mildly contagious 
disease, characterized by hemorrhagic inflammation and softening of the 
brain and spinal cord, often widespread, but sometimes limited to the 
anterior horns of the spinal cord; clinically it is characterized by fever 
and flaccid paralysis of one or more limbs. 

Etiology. — Poliomyelitis may occur sporadically or epidemically. Spo- 
radic cases occur widely distributed from time to time, but especially 
during the summer; they are almost exclusively confined in children 
from two to four years of age, although they do occur in older children. 
The epidemics have been most frequent in this country and in Norway. 
They have been more common in rural districts, but have occurred also 
in cities, such as New York, Christiania, Stockholm, etc. ; they have pre- 
vailed especially during the autumn ; and while many children have been 
affected, the disease has been quite common in young adults. 

The exciting cause of the disease has not been isolated. Flexner and 
Lewis, using an emulsion of the spinal cord from a fatal case in a child, 
have been enabled to transmit the infection to monkeys, and using the 
spinal cords of infected monkeys to transmit the infection to several 
generations of monkeys. Infections have been made successfully by 
intracerebral inoculation, and by inoculation into a large nerve (sciatic), 
into the circulation, into the peritoneum, and beneath the skin. The 
virus is filtrable (like that of rabies and vaccinia), and is believed to 
belong to the class of ultramicroscopic organisms. How the infection 
is acquired is not definitely known, although it is supposed to be by 
inhalation, the naso-pharynx being the primary site of infection. 

Pathology. — The lesions consist of inflammation, softening, and hemor- 
rhage, in mild cases, more or less limited to the anterior horns of the 
spinal cord, and leading to marked degeneration of the motor ganglion 
cells; the lesions, even in mild cases, however, may be more widespread 
and may be associated with lymphocytic infiltration of the pia-arachnoid. 
Analogous lesions may occur in the medulla, pons, and gray matter of 
the cerebrum. In severe cases the lesions are those of diffuse myelitis 
and encephalitis, with more or less meningitis, Flexner and Lewis 



EPIDEMIC POLIOMYELITIS 271 

have found the virus in the central nervous system, the cerebrospinal 
fluid, and mesenteric lymph nodes. After the disease has run its course, 
the affected portion of the cord is found lessened in size; the anterior 
horns are greatly atrophied and contain few if any ganglion cells; the 
corresponding motor nerve roots are atrophied; and the muscles supplied 
thereby are atrophic, sclerotic, and perhaps fatty. The lower motor 
neuron, therefore, bears the brunt of the infection. 

Symptoms. — The period of incubation is not known. There may be 
slight prodromal symptoms, but, as a rule, the onset is abrupt, with fever 
(101° to 103° F.), headache, malaise, perhaps vomiting, and rarely con- 
vulsions. In some cases pains are complained of in the arms, legs, or 
back; but, as a rule, attention is first directed to the limbs by paralyses. 
This develops rapidly, usually within twenty-four hours ; not infrequently 
the child, perhaps a little feverish on retiring for the night, is found 
paralyzed in the morning. The paralysis is, as a rule* at its maximum 
at the beginning, that is, usually it does not progress; it is irregular and 
asymmetrical in its distribution; it may involve a part of one limb, the 
entire limb, two or more, or all four limbs. In the legs the tibialis an- 
ticus and the extensors are most commonly involved; in the arm, there 
is an upper-arm type (deltoid, biceps, brachialis anticus, and supinator 
longus), and a lower-arm type (extensors or flexors of the wrist and fingers) 
— all of which is due to the group representation of muscles in the spinal 
cord. The muscles of the face (cranial nerves), the sphincters, and sen- 
sation are rarely affected. The reflexes are absent. The muscles sup- 
plied by the affected neurons soon undergo atrophy, become soft and 
flabby, and at the end of a week usually reveal the reactions of degener- 
ation. As a rule, after several weeks, some improvement takes place; 
in case there was only slight involvement of a limb, almost complete 
recovery may ensue ; but complete initial paralysis always results in more 
or less permanent disability. The limb remains smaller and shorter than 
its fellow, that is, growth is retarded; the muscles remain soft and flabby, 
and the skin cold and livid ; and contractures and deformities may ensue. 
In the case the leg is involved, apparatus are often required to enable 
the patient to get about. 

Diagnosis. — The diagnosis is readily made, fever and the rapid onset of 
flaccid paralysis in one or more limbs, soon followed by the reactions of 
degeneration, being unequivocal; these exclude the cerebral paralyses. 
The pseudoparalysis of infantile scurvy (acute rickets, scurvy-rickets) 
may be excluded by the usually complete loss of power and rapid atrophy ; 
in infantile scurvy, movement is possible although it is painful, and there 
are the characteristic changes in the bones, cutaneous hyperesthesia, etc. 

Prognosis. — The outlook is not hopeful; that is, complete restoration 
of structure and function is unlikely. The condition is usually at its worst 
in the first day or two; after a stationary period more or less improvement 
follows, but shortening, contractures, and deformities are common. 

Treatment. — If seen during the period of fever, the child should be put 
to bed and given a diuretic and diaphoretic fever mixture (spirit of 






272 INFECTIONS OF UNKNOWN ETIOLOGY 

nitrous ether, solution of ammonium acetate, or of potassium citrate, etc). 
The bowels should be freely opened ; and the affected limb or limbs may 
be wrapped in cotton wool. Starr recommends the use of hexamethy- 
lenamin, 1 grain (0.06 gram) every six hours, to a child three years of 
age; the drug is eliminated in the cerebrospinal tract and perhaps exerts 
some antiseptic action on the infectious microorganisms. Ergot, bella- 
donna, quinine, the salicylates, and potassium iodide have also been 
recommended. Attention must be paid to the general nutrition of the 
child — good food and fresh air. As soon as the sensitiveness has subsided, 
rubbing, kneading, and warm baths to the affected limbs should be insti- 
tuted; electricity is of less value, but may be employed. Strychnine is 
a serviceable remedy in this stage, and may be combined with other 
tonics. Deformities should be prevented by exercises and the use of 
orthopedic apparatus; developed deformities should be corrected, by 
operation if necessary. 



ACUTE INFECTIOUS JAUNDICE. 

(Weil's Disease.) 

From the large group of cases of infectious or toxic jaundice, a 
special form, known as Weil's disease, is usually separated, but the pro- 
priety of this is doubtful. Described by Weil, in 1886, it is character- 
ized by fever, jaundice, enlargement of the liver and the spleen, and 
nephritis. It prevails especially during the summer months, is most 
common in males between the ages of twenty and forty years, and seems 
to have a special predilection for butchers, soldiers, etc. It has been 
ascribed to Bacillus proteus fluorescens, which has been found in de- 
caying meat, sausages, drinking water, etc. Some French cases are 
ascribed to Bacillus coli infections'; others may be proteus infections. 
Doubtless all cases are not alike. Infection is. believed to be acquired 
by eating infected meat or cheese, or drinking tainted water. 

Pathology. — The tissues are bile-stained; the liver is normal in size or 
enlarged, the kidneys are swollen, and both organs exhibit fatty degener- 
ation of the epithelium, and the liver focal necroses; the spleen is 
enlarged; and hemorrhages into the skin and the mucous and the 
serous membranes may be encountered. 

Symptoms. — The onset is sudden, with chilliness, fever (103° to 104°F.), 
headache, malaise, rapid pulse, and severe neuromuscular pains, espe- 
cially in the back and the calves of the legs, but not infrequently also in 
the arms and even the cheeks. Jaundice develops on the second day; 
it is usually slight or moderate in degree, but may become severe; it lasts 
ten days or more, and gradually lessens. The liver is usually swollen 
and tender, the spleen is enlarged; the stools may be light colored, but 
commonly contain some bile; and the urine contains albumin and casts. 
Delirium and the typhoid state may supervene. With the onset of the 
jaundice the pulse becomes slower. Gastro-intestinal symptoms are 



FOOT-AND-MOUTH DISEASE 273 

unusual. The fever, which is characterized by marked remissions, lasts 
a week or ten days, and gradually subsides. Recovery usually ensues, 
but convalescence may be slow and relapses are not infrequent (40 per 
cent, of the cases, Quincke). 

Diagnosis. — In the diagnosis, other forms of infectious or toxic jaundice, 
catarrhal jaundice, and bilious remittent fever must be considered. 

Treatment. — The treatment is altogether symptomatic, and consists 
of rest in bed, a milk diet, cleansing of the intestine by calomel, the use 
of intestinal antiseptics, and the meeting of such other symptomatic 
indications as they may arise. 



FOOT-AND-MOUTH DISEASE. 

(Epidemic Stomatitis; Aphthous Fever; Epizootic Aphtha.) 

Foot-and-mouth disease, or epidemic stomatitis, is an acute, specific, 
infectious, and highly contagious disease of lower animals, transmissible 
to man, and characterized by a vesicular eruption on the oral mucous 
membrane and sometimes on the skin. 

Etiology. — Epidemic stomatitis is common among cattle, sheep, and 
pigs, and is transmissible to the domestic animals, and rarely to man, 
through the medium of infected milk, butter, or cheese; rarely infection 
occurs directly through a wound (hands, arm, foot). In cows the udders 
are not infrequently involved, whence the ready transference of the dis- 
ease through the medium of the milk. The specific etiological factor 
has not yet been isolated. Loftier, who has been able to vaccinate 
animals against the disease, believes that the specific cause is an ultra- 
microscopic organism, since it passes through porcelain filters the pores 
of which do not permit the passage of the smallest bacteria known. 

Symptoms. — The period of incubation is from three to seven days. 
The onset of the disease is announced by moderate fever, slight chilliness, 
a sensation of heat in the mouth and throat, pain and difficulty in swal- 
lowing, and soon the eruption of vesicles on the lips, oral, buccal, and 
pharyngeal mucous membrane, occasionally also on the skin, especially 
the hands (about the nails), the feet (between the toes), and rarely else- 
where. At the end of several days the vesicles rupture, and leave small 
ulcers that usually heal in a week or ten days. Rarely the exanthem 
is widespread, and has even been known to be hemorrhagic. Severe 
gastro-intestinal symptoms and endocarditis may occur as complications. 
The duration of the disease is two to four weeks. 

Diagnosis. — The diagnosis is easy; only the careless would mistake it 
for varicella. 

Treatment. — The treatment is that of stomatitis. If it be necessary 
to use the milk during the prevalence of an epidemic among the cows, it 
should at least be boiled. 
18 



274 INFECTIONS OF UNKNOWN ETIOLOGY 

MILIARY FEVER. 

(Swea ting Sickness . ) 

Miliary fever is an acute infectious and moderately contagious disease 
characterized by fever, profuse sweats, and a papulovesicular rash. 

Etiology. — The disease attacks children and adults apparently indis- 
criminately. It usually prevails epidemically — in Europe; as far as is 
known, no epidemic has occurred in this country. The exciting cause 
of the disease is not known. How the contagium is spread is not defi- 
nitely known, but the large number of persons affected at the one time 
lends support to the view of aerial convection. 

Symptoms.— The period of incubation is not definitely known, but it 
is probably not more than a day or two — during which there may be 
minor prodromal manifestations. As a rule, the onset is rather sudden, 
with fever and profuse sweating. The fever is usually not more than 
103° F., but hyperpyrexia has been observed. In addition, the patient 
complains of headache, respiratory oppression (suggesting suffocation), 
anorexia, and constipation. On the second or third day the character- 
istic rash appears — on the skin (often first on the face) and the oral mucous 
membrane; it consists of minute, reddish papules, most of which soon 
develop a tiny vesicle at their apex — much resembling sudamina. Suda- 
mina, that is, vesicles not on an inflammatory base, may also be observed. 
Soon after vesiculation, dessication, followed by desquamation, sets in. 
Sweating is constant, but exacerbations occur. In cases with high fever, 
other evidences of toxemia are present (delirium, prostration, etc.), 
and emaciation usually progresses rapidly. In favorable cases the fever 
falls by lysis, and by the tenth day the patient is convalescent. In un- 
favorable cases the patient dies with manifestations of increasing 
intoxication — delirium, coma, convulsions, hemorrhages, etc. In certain 
so-called fulminant cases death has occurred within the first few hours. 

Diagnosis. — In an epidemic the disease is unmistakable. 

Prognosis. — The mortality varies up to 25 per cent, in different epi- 
demics. Relapses are common. 

Treatment. — The treatment should consist of rest in bed, soft diet with 
a considerable amount of fluids (to replace the water lost by the sweats), 
hydrotherapy for its stimulating effect and to control the fever and 
toxemia, and stimulants (alcohol, strychnine, etc.); atropine may be 
indicated for the sweats. 



MILK SICKNESS. 

(Trembles.) 

Milk sickness is an acute infectious disease of cattle ("trembles"), com- 
municable to man, and characterized by gastrointestinal irritation and 
nervous phenomena attributable to toxemia, 



BERIBERI 275 

Etiology. — Trembles prevails among cattle, in the South and West, 
especially in newly settled regions, and is communicable to man and the 
young of horses and sheep. The specific infectious agent has not been 
isolated with certainty, although Jordan and Harris describe a so-called 
Bacillus lactimorbi. The infection is transmitted to man by means of 
milk, butter, and cheese; and these, as well as the flesh of infected cows, 
even after having been boiled, are poisonous to dogs. , 

Symptoms. — In cows, mild cases may be symptomless, unless the ani- 
mal is hard-driven, although the milk may be infectious; in severe cases 
the cow refuses food, the eyes become injected, the animal staggers and 
trembles all over, and may soon die, often in convulsions. In man the 
symptoms are gastro-intestinal, such as a swollen, coated, and tremulous 
tongue, fetid breath, thirst, epigastric distress and pain, nausea, vomit- 
ing and constipation; and toxic, such as fever, restlessness, coma and 
convulsions, or a typhoid state. Death may occur in two or three days 
in acute fulminant cases. In other cases the disease may last from ten 
days to about three weeks, and be followed by a tedious convalescence. 

Treatment. — The treatment is purely symptomatic. 

BERIBERI. 

(Kakke; Endemic Multiple Neuritis.) 

Beriberi is a specific, probably infectious or toxic, disease of tropical 
and subtropical countries characterized by multiple neuritis and different 
consequent motor and sensory paralyses, muscular atrophy, and ana- 
sarca. 

Etiology. — Beriberi is endemic in the Malay Archipelago, China, Japan, 
India, certain parts of South America (notably Brazil), the West Indies, 
the Dutch East Indies, the Philippines, and other South Pacific Islands. 
It is also occasionally met in different parts of the world, but largely 
as an imported infection. In this country it has prevailed especially 
among the Cape Cod fishermen, in asylums in Alabama and Arkansas, 
and in Louisiana. Bad hygienic surroundings, especially overcrowding, 
seem important etiologically, whence the frequent occurrence of the 
disease in barracks, jails, ships, etc.; but marked heat and humidity 
seem also to be of significance, whence its frequent occurrence during 
the rainy season. The yellow races are particularly susceptible. Males 
are more frequently affected than females, largely because of extraneous 
circumstances. The disease is most common during adolescence and 
early adult life — the fifteenth to the fortieth year. 

The exciting cause of the disease has not been determined. There is 
considerable, though not conclusive, evidence that it is due to micro- 
organismal infection, as maintained by Baelz, Scheube, and W r right, the 
last mentioned of whom believes that the infecting organism gains 
entrance to the body through the mouth and elaborates its toxin in the 
stomach and duodenum. Okata and Kokubo have described a coccus 
which they have isolated from the urine and which they believe is the 



276 INFECTIONS OF UNKNOWN ETIOLOGY 

specific cause. The Japanese generally attribute the disease to bad 
food, especially rice and fish, which either itself directly causes the dis- 
ease (whence a nutritional disorder due largely to deficient nitrogen 
supply or assimilation) or acts as the carrier of the infection or toxin. 
Ross attributes it to arsenical poisoning, since arsenic is a common 
adulterant of tobacco in the East, and he has found arsenic in the hair 
of a number of patients. 

Pathology. — The characteristic lesions consist of degeneration of 
the peripheral nerves, involving the axons and medullary sheaths. In 
severe cases, similar lesions are found in the pneumogastric and the 
phrenic nerves. There is also congestion of the pylorus of the stomach 
and of the duodenum (considered specific by Wright), hyperemic and 
cloudy swelling of the liver and the kidneys, enlargement of the spleen, 
and parenchymatous and fatty degeneration of the cardiac and the volun- 
tary muscles; and in some cases oedema of the subcutaneous tissues and 
serous cavities. 

Symptoms. — The period of incubation is not known, but it has been 
said by Wright to be between ten and fifteen days. Clinically, Scheube 
distinguishes four types of the disease — largely variations in degree : 

The rudimentary form begins usually with pain and weakness in 
the extremities, associated with paresthesia and anesthesia of the leg, 
frequently quite circumscribed and irregular in distribution. Slight 
oedema also may develop, the muscles may become tender, and palpita- 
tion of the heart, dyspnoea, and abdominal uneasiness may be observed. 
The symptoms last for a few days to several months, and generally 
disappear. Recurrences, however, are often encountered. 

The paralytic or atrophic form presents, as a rule, symptoms similar 
to the foregoing, but the pains in the limbs are more pronounced, and 
the muscles of the legs soon become paralyzed and atrophic. The par- 
alyses and atrophy may extend to the muscles of the trunk, less frequently 
to the arms, head, and neck. The paralyses are usually flaccid, reactions 
of degeneration are present, and the tendon reflexes are absent. The 
areas of anesthesia and of paresthesia are often irregularly distributed. 
The cardiac symptoms are not pronounced, and the oedema is usually 
slight (whence the term, dry beriberi). Recovery, when it ensues, is 
very slow. 

The dropsical form begins as the preceding forms, but oedema soon 
appears, and the patient, as a rule, speedily becomes anasarcous — effusions 
into the subcutaneous tissues and the serous cavities. Palpitation of the 
heart, rapid heart action, dyspnoea, and cyanosis of the extremities are 
quite marked. Paralyses and muscular atrophy are not as pronounced 
as in the other cases, but even notable atrophy is not infrequently ob- 
scured by the existing cedema. The urine is diminished in amount, 
but, as a rule, contains no albumin. The condition persists for weeks 
and even months, and if recovery eventually ensues there is sometimes 
a very rapid disappearance of the cedema, with great increase in the 
amount of urine. 



EPIDEMIC DROPSY 277 

The acute pernicious or cardiac form begins as the preceding forms, 
but cardiac weakness is soon manifest, and complete cardiac failure may 
supervene within twenty-four hours. Usually, however, it lasts several 
weeks. 

Diagnosis.— The disease where it is endemic presents no diagnostic 
difficulties, especially when several cases exist in the same vicinity. In 
sporadic cases, evidences of peripheral neuritis, with anasarca, and an 
irritable and weak heart, in a patient just arrived from the tropics is 
extremely significant. Arsenical and alcoholic neuritis should be ex- 
cluded. 

Prognosis. — The mortality varies from 2 per cent, in mild cases to 40 
per cent, in severe cases. Patients seemingly progressing favorably not 
infrequently die of acute cardiac failure. 

Treatment. — The patient should be removed from the endemic locality, 
be placed amidst the best hygienic surroundings, and given a diet rich 
in nitrogen and phosphorus. The treatment otherwise is largely symp- 
tomatic. Stimulants are valuable for cardiac weakness. Acute cardiac 
failure should be met with bleeding and free purgation. During conva- 
lescence the neuritis is to be treated as any other neuritis. Baelz has 
recommended the salicylates in the early stages of the disease. 



EPIDEMIC DROPSY. 

Epidemic dropsy is a subacute, infectious, and contagious disease 
characterized by fever, vomiting, diarrhoea, and the sudden appearance 
of anasarca. 

Etiology^ — Epidemic dropsy is peculiar to India, where it prevails 
especially during the cold weather, and attacks adolescents and adults 
of both sexes. It is rare in infants. The exciting cause of the disease 
has not been isolated, though there is some evidence that the contagium is 
more or less readily communicable from the sick to the well. 

Symptoms. — The onset of the disease is often marked by fever, varying 
from 99° to 102° F., which often precedes but sometimes accompanies 
the development of dropsy — the most characteristic feature of the 
disease. Vomiting and diarrhoea are common, and sometimes mark 
the development of the disease. The dropsy begins, as a rule, in the 
legs, and soon involves the entire body; it may be preceded by 
burning, pricking, and itching of the skin. Marked anemia soon 
supervenes, and disturbances of circulation and respiration are prominent 
in almost all cases. An erythematous rash often appears on the face 
and trunk about a week after the development of the dropsy. The dis- 
ease runs its course in from three to six weeks. The mortality varies 
from 2 to 40 per cent., and death results from oedema of the lungs, 
hydrothorax, hydropericardium, or other cardiac or pulmonary com- 
plications. 

Treatment. — The treatment is purely symptomatic. 



278 INFECTIONS OF UNKNOWN ETIOLOGY 

NASHA FEVER. 

(Nakra Fever.) 

Nasha fever is an acute infectious disease, peculiar to certain parts 
of India, especially Bengal, and characterized by fever, swelling of the 
nasal mucous membrane, and sometimes coma and death. 

Etiology. — The nature of the disease is not known. Exposure, un- 
hygienic conditions, and poor food seem to predispose to it. Women 
apparently are more predisposed than men; children and the aged are 
relatively immune. It prevails mostly from April to August. One attack 
seems to predispose to others, which sometimes develop at more or less 
definite intervals. The disease is believed by some observers to be a 
manifestation of malaria, but this is doubtful, since the malarial parasite 
has not been found and the disease is refractory to quinine. 

Symptoms. — The disease usually begins with congestion of the nasal 
mucous membrane and the development of a pea-sized, circumscribed 
swelling on the nasal septum. The patient soon complains of malaise, 
headache, severe neuromuscular pains in the neck and shoulders, con- 
stipation, and fever. The fever is moderate in degree and usually sub- 
sides in from three to five days, concurrently with subsidence of the nasal 
symptoms. The swelling of the nasal mucous membrane never goes 
on to suppuration, but cases have been reported in which sudden sub- 
sidence of the swelling has been followed by grave cerebral symptoms, 
such as coma, delirium, and death. The spleen is usually enlarged and 
palpable. A diffuse erythematous eruption has occasionally been 
observed. 

Treatment. — The treatment is purely symptomatic. Puncture of the 
spleen, which has been recommended as affording relief to the local and 
general symptoms, seems to be unduly hazardous. 



JAPANESE RIVER FEVER. 

Japanese river fever is an acute, infectious disease, occurring in the 
western part of the Island of Nippon, and characterized by an initial 
eschar, soon followed by ulceration of the skin, continued fever, inflam- 
mation of the lymphatics, and an exanthematous eruption. 

Etiology. — The nature of the disease is unknown, though it affects 
practically only those engaged in harvesting the corn and hemp in 
a certain part of the island of Nippon. The Japanese attribute it to the 
bite of an ascarus. The primary eschar is not unlikely the point of 
infection. Sex and age are without etiological influence. One attack 
does not confer immunity, though it seems to lessen the severity of sub- 
sequent attacks. 

Symptoms. — The period of incubation is from four to seven days, 
during which the patient may complain of malaise and repeated rigors. 



PONOS 279 

The first indication of the disease is the initial eschar, which develops 
about the genitals, the axillae, or the neck. Soon an ulcer forms — round, 
dark, tough, firmly adherent, and surrounded by a painless area of super- 
ficial congestion. The regional lymph nodes, and sometimes all the 
lymph nodes of the body and the spleen, become swollen and con- 
gested. With the onset of the infection, fever develops, pursues a 
more or less continued course, and ranges between 103° and 104° F. 
Catarrhal inflammation of the conjunctivae and of the bronchi not in- 
frequently arises. On about the fifth to the seventh day an eruption, 
consisting of large, dark red papules, appears on the face, forearms, 
legs, and trunk, and not infrequently at the same time a minute lichenous 
rash appears on the forearms and trunk. Both eruptions disappear 
in from four to seven days, while the fever begins to remit at the end 
of about two weeks, and the temperature soon reaches the normal. 
During the second week the ulceration begins to heal, the eschar being 
first cast off. The mortality varies between 15 and 50 per cent. 

Treatment. — The treatment is purely symptomatic. The ulcer should 
be dressed antiseptically. Quinine and the salicylates have been recom- 
mended internally. Hydrotherapy also may be useful. 



PONOS. 

Ponos is a rare, chronic, endemic disease of childhood that occurs 
in the islands of Spetza and Hydra, off the coast of Argolis, and is char- 
acterized by irregular fever, enlargement of the spleen, and emaciation. 

Etiology. — Apparently ponos effects only children, and commonly 
those under the age of four years, and of tuberculous antecedents. It 
appears to be uninfluenced by climate, season, or social conditions. 
Its exciting cause is not known, and in reality its nature is ill understood. 

Pathology. — Apparently the necrospy findings of only one case have 
been reported. In this the spleen was much enlarged, the capsule firm, 
and the stroma and trabecular considerably thickened; the liver exhibited 
early cirrhosis; the kidneys were congested; and the bronchial and the 
mesenteric lymph nodes were swollen. 

Symptoms. — The onset is sudden with fever, which, having developed, 
pursues a remittent and irregular course. The spleen rapidly enlarges 
and becomes tender; dyspepsia and constipation develop, and the patient 
emaciates rather rapidly. When the disease has become well established 
oedema and ascites may develop, and hemorrhages into and from the 
different organs and tissues, especially the gums, may occur. Boils 
and superficial areas of gangrene have been observed. The disease 
lasts for a few months to several years, and the patients rarely recover. 

Treatment. — The treatment is unsatisfactory and scarcely more than 
symptomatic, consisting largely of careful dieting and the administra- 
tion of tonics. 



280 INFECTIONS OF UNKNOWN ETIOLOGY 



HILL DIARRHOEA. 

Hill diarrhoea is a peculiar disorder of the tropics, especially India, 
characterized by morning diarrhoea, copious, pale, liquid stools, and 
flatulent dyspepsia. 

Etiology. — The causative factors of hill diarrhoea are ill understood. 
The disorder is especially common in colonists who, having become 
acclimated to low, hot plains, go (often for a holiday) to the neighboring 
hills (5000 feet or more). The disease seems to be more than an ordinary 
intestinal catarrh; in some respects it resembles sprue, though, unlike 
it, it tends to recovery. By some observers it is believed to be dyspeptic 
in character and associated with suppression of the function of the liver, 
pancreas, etc. Scheube attributes it to atony of the colon, and to chilling 
of the abdomen due to the cold and dampness of the early morning hours 
of tropical mountainous countries. 

Symptoms. — The disorder not infrequently begins with flatulent 
dyspepsia soon after the subject reaches the mountains. Usually on 
the following morning between 3 and 5 o'clock diarrhoea begins, and 
from six to twelve stools or more may be passed before noon, after 
which the diarrhoea not infrequently ceases for the remainder of the day. 
The stools are copious, watery or pasty, pale, frothy, and have been 
likened to whitewash (they contain no biliary coloring matter). The 
stools are, as a rule, unattended by pain or tenesmus, though there may 
be a vague, indefinite tenderness along the course of the colon. The 
abdomen is sometimes markedly distended, and there may be consider- 
able borborygmi. The disease tends to recovery at the end of ten days 
or two weeks. Recurrences may attend repeated visits to the hills. 

Diagnosis. — Manson states that the distinctive features of the disease 
are the regular recurrence of morning diarrhoea, its cessation after a 
certain hour in the forenoon, the absence of color in the stools, and the 
attendant flatulence. 

Treatment. — The diet in the majority of cases should consist of milk, 
though one can readily understand that some patients might do better 
on animal broths, etc., that have less tendency to ferment. The patient 
should remain in bed during the morning hours, and should be warmly 
clad. Calomel is believed to be useful to stimulate the hepatic function. 
Crombie and Manson advise a teaspoonful of Liquor hydrargyri per- 
chloridi (B. P.), in water, fifteen minutes after each meal. The digestive 
ferments are sometimes useful. If treatment is of no avail, the patient 
should return to the lowlands whence he came. 



EPIDEMIC GANGRENOUS PROCTITIS 281 



SPRUE. 

(Psilosis; Chronic Diarrhoea of Warm Climates; Chronic or Endemic Diarrhoea of 
Cochin China; Tropical Diarrhoea; Ceylon Sore Mouth; Cachexia Aphthosa.) 

" Sprue, or psilosis, may be defined as an insidious, chronic, remitting 
inflammation of the whole or part of the mucous membrane of the ali- 
mentary canal, occurring principally in Europeans who are residing or 
have resided in tropical or subtropical climates. It is characterized by 
irregularly alternating periods of exacerbation and comparative quies- 
cence; a peculiar inflamed, superficially ulcerated, exceedingly sensitive 
condition of the mucous membrane of the tongue and mouth; great 
wasting and anemia; pale, copious, and often loose, frequent, and frothy 
fermenting stools; very generally by more or less diarrhoea; and also 
by a marked tendency to relapse. Sprue may either be primary, or it 
may supervene on or complicate other affections of the alimentary canal. 
Unless properly treated it is usually fatal." (Manson.) 

Etiology. — The cause is unknown. The anatomical lesions are not 
characteristic. 

Treatment. — The treatment is largely hygienic and dietetic. Manson 
prefers an exclusive milk diet for weeks or months; others prefer a 
meat diet. 

EPIDEMIC GANGRENOUS PROCTITIS. 

Epidemic gangrenous proctitis is an acute infectious disease, character- 
ized by rapidly spreading phagedena of the anus and rectum, progressing 
to prolapse and gangrene of the ulcerated rectum. 

Etiology. — Epidemic gangrenous proctitis is more or less widely 
distributed throughout the tropics, but it is especially prevalent in 
Central and South America, and in the Philippines and other Pacific 
Islands. Its exciting cause is not definitely known, but it has been 
attributed to bacterial infection (Bacillus dysenterise, Bacillus pyocy- 
aneus, etc.), and in Venezuela to the eating of the green stalks of unripe 
maize. The latter view, however, is scarcely tenable (for all cases at 
least), since the disease occurs where maize does not exist. The develop- 
ment of the disease seems favored in low-lying, damp regions. In 
South America it is almost confined to children; in other tropical regions 
adults also are attacked. 

Pathology. — The lesions consist of ulceration attended by pseudo- 
membranous formation, limited in some cases to the region of the 
sphincters, but often spreading to the rectum and the sigmoid, and soon 
followed by prolapse and gangrene of the rectum. 

Symptoms. — The initial symptoms consist of burning and itching 
above the anus and a tendency to frequent defecation. Soon the dis- 
charges become more frequent and are attended by abdominal pain and 
constant and distressing tenesmus, which frequently leads to extrusion 



282 INFECTIONS OF UNKNOWN ETIOLOGY 

of the bowel. Fever, anorexia, and thirst supervene. The stools at 
first consist of fecal matter; soon, however, they become mucoid or muco- 
sanguineous, and extremely fetid. Occasionally even almost pure blood 
is discharged. Severe nervous symptoms, such as delirium and coma, 
and in children, convulsions, supervene. The patient emaciates rapidly, 
and, as a rule, soon dies — in some cases before prolapse of the rectum 
has occurred. Recovery, however, occasionally ensues, even after the 
advent of coma, prolapse, and gangrene (with sloughing) of the rectum. 

Diagnosis. — In the early stages the disease is not unlikely to be mis- 
taken for dysentery, but an examination of the anus and rectum serves 
to prevent error. 

Treatment. — Opium is indicated to relieve pain and to control the 
intestinal movements. It may be given hypodermicly, but should also 
be applied locally to the inflamed and ulcerated areas. Antiseptic and 
soothing lotions to the anus and rectum are also called for. The local 
use of a portion of roasted lemon or of lemon juice has a vogue in Vene- 
zuela. In the event of gangrene the rectum must be excised, should the 
patient's condition warrant it. 



TROPICAL PHAGEDENA. 

Tropical phagedena is a rapidly spreading gangrene of the skin and 
subcutaneous tissues, leading to the formation of a large sloughing sore. 

Etiology. — Tropical phagedena is preeminently a disease of the tropics, 
occurring especially where the climate is hot and damp. The exciting 
cause of the disease is not known, though doubtless it is a microorganism. 
It finds its readiest victims among the physically depressed and those in 
poor health from any cause. In some subjects an insect bite or an abra- 
sion seems to be the starting point of the infection. 

Symptoms. — The feet and legs are the most common seat of the 
lesions, though no part of the body is exempt. The first indication of 
the disease, if the skin has been previously sound, is the development of 
a large blister, containing a serosanguinolent fluid. This ruptures in 
a few hours, and exposes a sloughing sore which rapidly spreads and 
forms a horribly fetid, yellowish ulcer, the centre of which liquefies 
in a few days, while the periphery continues to spread. Not only is 
there peripheral extension, but also extension in the depths, whereby 
the muscles, tendons, nerves, vessels, and bone may become implicated. 
At the end of a week or more the slough is gradually separated. When 
the disease begins in an already existing wound or sore, the granulating 
surface dries and is gradually converted into a slough. 

The lesions cause considerable pain which, together with the drain on 
the system, undermine the patient's health, and may lead to death from 
exhaustion, hemorrhage, or septicemia. In some cases, however, the 
constitutional disturbance is relatively slight and cicatrization proceeds 
— provoking, as a rule, considerable deformity and mutilation. 



ULCERATING GRANULOMA OF THE GENITALS 283 

Treatment. — Opium is indicated not only to relieve pain, but also 
because of a seeming beneficial action on the phagedenic process. 
The ulcer should be curetted or cauterized with pure carbolic acid, and 
then continuously irrigated with a tepid antiseptic lotion. The general 
health should be maintained by tonics and nutritious food. 



TROPICAL BUBO. 

(Climatic Bubo; Tropical Non-venereal Adenitis.) 

Tropical bubo is a non-venereal inflammatory enlargement of the 
inguinal lymph nodes attended by remittent fever lasting from three 
to four weeks. 

Etiology. — Tropical bubo is most common in the East Indies and China, 
but occurs also in South Africa, Japan, the Philippines, along the coast 
of the Mediterranean Sea, in the West Indies, Malaga, etc. Limited 
epidemics have been observed among sailors and soldiers. Age is of 
no etiological importance. The exciting cause of the disease has not 
been isolated, though it is doubtless microorganismal. Infection is 
believed to occur through small wounds or abrasions of the legs or genitals 
or through the bites of insects. 

Symptoms. — The onset of the disease is often rather sudden, with 
chill, fever (103° to 104° F.), headache, backache, and enlargement, 
tenderness, and redness of the lymph nodes of the groin of one or 
both sides. In some cases a group of nodes, in other cases separate 
contiguous nodes, are involved. The nodes increase in size until 
they attain that of a goose egg, whereupon the fever, which has been 
remittent in type, gradually lessens and the nodes decrease in size — 
though they may remain enlarged for two months or more. Usually 
there is little pain, and the constitutional symptoms, aside from the fever 
are slight. In some cases, however, the skin over the enlarged nodes 
becomes adherent, and the nodes soften and form suppurating sinuses, 
which lead not only externally but often deeply into adjacent tissues. 
In this event the pain and constitutional symptoms may become marked. 
The suppuration may continue several months. 

Treatment. — If softening has not occurred, iodine and ichthyol, or 
an ointment of mercury, belladonna, and iodine, may be applied. If 
softening occurs, the abscess should be opened freely, curetted, and treated 
antiseptically. General treatment is rarely called for, and at all events 
is to be based upon general principles. 



ULCERATING GRANULOMA OF THE GENITALS. 

Ulcerating granuloma of the genitals (pudenda) is a chronic venereal 
disease of the tropics, characterized by its granular character, its large 
extent, and its tendency to hemorrhage. 



284 INFECTIONS OF UNKNOWN ETIOLOGY 

Etiology. — Ulcerating granuloma of the genitals occurs in men and 
in women between the ages of thirteen and fifty years, and is uninfluenced 
by sex. The exciting cause has not been isolated, though it is present in 
the secretions from the granulations which are auto-inoculable and in- 
fectious to others. Wise has demonstrated spirochetes (resembling Spiro- 
chseta refringens) in the secretions. 

Symptoms. — The disease begins on the genitals as an insignificant 
circumscribed nodular thickening and elevation of the skin, which soon 
develops into a light red, shiny mass of granulation tissue (partaking of 
the nature of the infectious granulomas) ; this has a fetid odor, excretes 
a thin, sanguineous fluid, and bleeds readily. The warm, moist surfaces 
about the scrotum, or the labia, and the thighs, are most susceptible 
of infection. The lesions spread slowly by peripheral extension, as well 
as by auto-inoculation of opposed (and other) surfaces, and involve 
most frequently the scrotum, the perineum, the glans penis, and the upper 
part of the thighs in the male, and the labia, the vagina, and the upper 
part of the thighs in the female. Spontaneous recovery is unusual, 
though not infrequently attempts at healing are seen — gradual shrinkage 
and the formation of a thin, somewhat raised, cicatrix, which, however, 
having formed, not uncommonly breaks down again. 

Treatment. — Complete excision is the best treatment if the lesions 
are not too extensive — in which event the granulation tissue should be 
curetted and cauterized. 

VERRUGA. 

Verruga is a chronic infectious disease, characterized by initial (so- 
called) rheumatoid pains, fever, anemia, and the development of 
peculiar, warty, granulomatous, protuberances on the skin, mucous 
membranes, and the internal organs. 

Etiology. — Verruga is most prevalent in Peru (whence it is often called 
verruga peruana), on the Pacific slope of the Andes Mountains, and 
in certain of the mountainous regions of Chili, Bolivia, and Ecuador. 
It occurs in both sexes, at all ages, and is apparently favored by moisture, 
heat, and elevation (since it is scarcely if ever observed at the level of 
the sea). It occurs in circumscribed epidemics, but is not markedly 
contagious. The exciting cause has not been isolated. How infection 
is spread is not known, though the natives of Peru attribute it to the 
water of certain springs. Malaria is frequently associated, and is 
believed by some to be of etiological significance. One attack confers 
immunity. 

Symptoms. — The period of incubation is usually from fifteen to 
forty days, though rarely it may be longer or even shorter. Clinically 
two well-defined stages are recognized — that of invasion and that of 
eruption. The onset is usually insidious and marked by lassitude, 
indisposition, neuromuscular pains in the legs, followed in a few days by 
slight rigors and evening fever, which soon increase in severity. The 



KUBISAGARI 285 

fever may reach 102° to 103° F., and pursues usually a remittent, but 
occasionally an intermittent course. The fever is accompanied by 
insomnia, intense headache, hemorrhages, and pains in the back and 
the joints, of which the knee, ankle, and the small joints of the hands 
and feet are most susceptible. 

Spasmodic and painful contractures of certain muscles, especially 
of the calves and of the neck, occur — most frequently at night. Nausea, 
vomiting, vertigo, photophobia, transient amblyopia, dyspnoea, bronchitis, 
loss of appetite, and marked thirst are also commonly complained of. 
Early in the disease the bowels are constipated, but later diarrhoea 
develops. Marked anemia and emaciation soon supervene, and con- 
stitute characteristic features of the disease. The liver is frequently, 
the spleen less commonly, enlarged and palpable. The fever gradually 
subsides in about thirty days (more or less) and therewith the stage of 
eruption sets in. This consists at first of pin-sized pinkish papules, 
which gradually become darker (somewhat bluish) in color, and increase 
in size until they form quite large excrescences. Manson originally 
regarded them as identical macroscopically and microscopically with 
the granulomas of yaws, but more recently other observers, notably 
Glogner, have pointed out noteworthy differences. As in yaws, how- 
ever, the eruption may be sparse or abundant, discrete or confluent; 
and the swellings or granulomas are exceedingly vascular and bleed 
freely, thus contributing to the anemia. They are found most commonly 
on the face, neck, and limbs; in many cases they develop on the palms 
of the hands, the soles of the feet, and the hairy scalp — while the trunk 
is usually exempt; they are common also on the mucous membranes, 
and in the different organs of the body, where they often occasion notable 
hemorrhages. The lesions persist from four to six weeks, and then desic- 
cate and desquamate, or sometimes undergo ulceration and suppuration. 

Prognosis. — Among natives the mortality is from 10 to 15 per cent.; 
it is much higher among the white race, and may reach 60 to 70 
per cent. 

Diagnosis. — Though verruga much resembles yaws, it can usually 
be distinguished by the involvement of the internal organs, which are 
unaffected in yaws, and by the marked tendency to hemorrhage mani- 
fested by the lesions. 

Treatment.- — Treatment, aside from removal from mountainous regions 
to the coast, which is indicated in all cases, is purely symptomatic. 
Quinine has been recommended on account of the common association 
of malaria. The removal of the ulcerated areas has also been practised. 



KUBISAGARI. 

(Endemic Paralytic Vertigo.) 

Kubisagari is a chronic endemic disease of the northeastern part of 
the principal island of Japan, characterized by dimness of vision, 



286 INFECTIONS OF UNKNOWN ETIOLOGY 

diplopia, ptosis, and paralysis of certain muscles, especially of the neck 
(whence the name, kubisagari, that is, one who hangs his head). 

Etiology. — The nature of the disease is ill understood. It is almost 
confined to farming peasants, especially those who live under the same 
roof with their cattle, in which, as well as in many other respects, it re- 
sembles endemic paralytic vertigo (Gerlier's disease) of Switzerland and 
certain parts of France. Miura believes that the local horse plague 
and cattle plague are in some way related etiologically to the disease. 
Age and sex are without influence. The disease is most common during 
the warm season, and disappears during the winter. 

Symptoms. — Kubisagari is characterized by attacks which come on 
at intervals of several hours to several days, and last for from several 
minutes to several hours, during which there is dimness of vision, diplopia, 
ptosis, and paralysis of different muscles. Paralysis of the posterior 
cervical muscles is the most common, and causes the head to drop for- 
ward; paralysis of the muscles of the tongue, of the lips, of the cheek, 
and of deglutition interferes with speech, mastication, and swallowing; 
and paralysis of the muscles of the trunk and the extremities, which 
is less common, interferes with station and locomotion. The attacks 
sometimes come on without known cause, but in some cases are induced 
by physical exertion (especially, it is said, a stooped posture with the 
stomach empty), by hunger, by indigestion, by eye-strain, etc. In 
some cases there is considerable mental depression; the lacrymal, 
nasal, and salivary secretions may be increased; and the reflexes may 
be exaggerated. The disease is not fatal, though it may last for 
years. 

Treatment. — Treatment, as a rule, is not encouraging. Miura re- 
ports favorable results from the use of potassium iodide and arsenic, 
and the bromides are believed to be sometimes of some avail in controlling 
the frequency of the attacks. 



GANGOSA. 

Gangosa is a disease that prevails in Guam, where it is said to involve 
about two per cent, of the population; it occurs also in the Ithmus of 
Panama, the West Indies, the Philippines, and perhaps in certain parts 
of South America. It is described by Mink and McLean as being 
characterized by a destructive ulceration, usually beginning on the soft 
palate, pillars, or uvula, and extending by continuity to the hard palate, 
the nasal cavity, the larynx, and even the face. Active ulceration is fol- 
lowed, after a variable period, by cicatrization or chronic ulceration. 
Mutilation always results. Constitutional symptoms are either slight or 
absent. The disease resembles, but may readily be differentiated from, 
leprosy, syphilis, tuberculosis, etc. A specific infectious agent has not 
been isolated; but the disorder appears to be infectious, being spread by 
contact. 



PSITTACOSIS 287 



AINHUM. 



Ainhum is described by Manson as a disease affecting the toes, espe- 
cially the little toes, of negroes, East Indians, and other dark-skinned 
races, and commencing as a narrow groove in the skin, almost invariably 
on the inner and plantar side of the foot of the little toe, of one or both 
feet. Once started, the groove deepens and extends gradually around 
the whole circumference of the toe; the distal portion of the toe is likely 
to swell to a considerable size, as if constricted by a ligature. There is 
little or no pain, although there may be inconvenience from the liability 
to injury of the dangling and everted toe. In the course of years the 
groove deepens, and finally the toe drops off as if amputated. The dis- 
ease has been variously interpreted — as being a manifestation of leprosy, 
a circumscribed scleroderma, a trophoneurosis, a congenital spontaneous 
amputation, the result of self-mutilation by ligatures, wearing toe rings, 
etc., and as caused by injuries to the toes. Wellman believes that it 
results from injuries to bare-footed persons, caused by long grasses, and 
that the factor in prolonging the irritation and inflammation is the chigger, 
Sarcopsylla penetrans, which seems to have a predilection for the affected 
spot, especially if the skin be cut or torn. 

GOUNDOU. 

(Anakhre.) 

Goundou is a disease that occurs among the natives of Africa, and is 
characterized by severe and persistent headache, later followed by a 
sanguinopurulent discharge from the nostrils, and the development of 
painless symmetrical swellings at the sides of the nose. Although the 
discharge may subside, the swellings progressively increase in size until 
they may be as large as an ostrich's egg; eventually they may obstruct 
the line of vision or destroy the eyes. The disease has been variously 
interpreted as a manifestation of yaws, or of syphilis, as a malformation 
due to the non-union of the nasal and frontal bones, as a manifestation 
of atavism referable to tribal peculiarities of the original negro, as a 
disease sui generis, and as a disease caused by the larva? of insects in the 
nostrils. Wellman believes that the growths are due to an osteoplastic 
periostitis, the definite cause of which has not been demonstrated. 

PSITTACOSIS. 

Psittacosis is a disease of birds, characterized by loss of appetite, 
general weakness, diarrhoea, and death (often in convulsions). It is 
believed to be communicable to man, infection being commonly acquired 
from parrots — in England, Germany, France, and Italy. In man it is 
characterized by pneumonia that is often atypical in course, attended by 
toxemia, and usually ends fatally. 



SECTION II. 
INTOXICATIONS. 



The intoxications to be here discussed comprise the series of diseased 
conditions, the result of more or less continued activity of divers poison- 
ous chemical substances; the acute poisonings belong more properly to 
the subject of toxicology. 

ALCOHOLISM. 

Symptoms. — Acute Alcoholism. — The effect of a large amount of 
alcohol taken within a short time is exerted chiefly on the nervous 
system; at first there is exaltation of the nervous functions, which is soon 
followed by perversion, and finally depression and stupor. In the ordi- 
nary case the action of the heart becomes at first accelerated, respira- 
tion quickened, the muscular force and activity increased, the mentality 
active, the eyes brilliant, and the face flushed (although it may be pale); 
the patient gradually becomes loquacious and indiscreet in his confi- 
dences, and care fades away. Soon, however, the perceptive faculties 
become confused, the intellect dulled, the memory faulty, movement 
of the limbs uncertain and incoordinate, the gait unsteady, the speech 
thickened, the facial flush deepened, the pupils dilated, the conjunctivae 
red and watery, and the gaze staring. Gradually depression of the gen- 
eral functional activities ensues, and the patient passes into a more or less 
profound sleep (from which, however, he can be more or less aroused); 
the temperature may become subnormal. In other cases the subject 
becomes readily infuriated or maniacal, and upon slight or no provoca- 
tion may commit serious crimes, such as murder, etc. Periodical recur- 
rences of such attacks of acute alcoholism are common in persons with 
an inherited or acquired craving for alcohol — so-called dipsomaniacs; 
in the intervals between attacks the subject may abstain entirely from 
alcohol. The ordinary attack of acute alcoholism is readily recognized, 
but alcoholic coma must be distinguished from apoplexy, uremia, dia- 
betic coma, morphine poisoning, etc. 

Chronic Alcoholism. — While it is undoubtedly true that many 
persons can take a moderate amount of alcohol (whiskey, wine, beer) 
and attain a ripe old age in good physical condition, the matter is 
19 



290 INTOXICATIONS 

largely individual, and to the majority of mankind the continuous or 
daily consumptiom of even a moderate amount of alcohol is fraught 
with danger. Alcohol brings inevitably in its wake disordered function 
and altered structure. The bloodvessels become sclerosed, and the 
heart hyper trophied and dilated or fatty; the gastro-intestinal tract 
becomes congested and chronically inflamed, giving rise to the so-called 
morning sickness of alcoholics — anorexia, nausea, perhaps vomiting, 
coated tongue, constipation, etc.; the liver becomes cirrhotic; the kid- 
neys become the seat of chronic diffuse indurative nephritis; and the 
nervous system reveals various deteriorations. Of these, muscular 
tremor, involving the extremities, especially the hands, the lips, and the 
tongue, are common; various disorders of sensibility, including the 
special senses, neuralgiform pains and true neuritis, meningitis, etc., 
may develop. The mind (will and intellect) and the morals deteriorate. 
The patient becomes irritable and suspicious; his judgment becomes 
impaired, his memory enfeebled, and sleep unsatisfying; lapses from 
moral rectitude (sexual and other) are common; hallucinations and 
delusions may supervene, and the patient may gradually pass into 
irremediable insanity. The association in chronic alcoholics of loss 
of memory, pseudoreminiscences (false notions as to time, place, 
and actualities), and peripheral neuritis is spoken of as Korsakoff's 
psychosis. 

Delirium Tremens (Mania a potu). — Delirium tremens is an inci- 
dent of chronic alcoholism, that usually follows periodical excessive 
indulgence in alcohol, and may be precipitated by a fright, shock, frac- 
ture, or other trauma, acute infection, especially pneumonia, etc. The 
symptoms usually begin with general restlessness, mental activity 
(sometimes apathy), and insomnia — for which additional alcohol may 
be taken — without avail. In two or three days delirium and halluci- 
nations of sight and hearing set in. The patient talks incessantly and 
incoherently; conducts imaginary enterprises, and insists upon their 
urgency, so that unless watched or restrained he avails himself of the 
first opportunity to escape from his bed and room — usually by way of 
the window. Should he doze, he may be awakened by terrifying dreams, 
and while awake he is tormented by the most distressing hallucinations 
— of sight, such as rats, mice, demons, snakes (a patient of mine with 
marked aortic insufficiency was assured of being infected with snakes 
by watching the violent pulsations of his very tortuous arteries in the 
arms); and of hearing, insulting remarks, threats of imaginary enemies, 
etc. There is a well-marked muscular tremor; the pulse is rapid and 
soft, often very weak; and there may be some fever, which, however, 
is almost if not always due to a complication, such as pneumonia, which 
is often overlooked. In favorable cases, at the end of three to five days 
the patient sleeps, the restlessness abates, the hallucinations disappear, 
and the patient begins to convalesce. Very noticeable improvement often 
follows a prolonged sleep, but the tremor may continue for some time. 
In unfavorable cases with increase of the symptoms and persisting 
insomnia the patient dies of exhaustion. 



ALCOHOLISM 291 

Treatment. — The ordinary and recurring attacks of acute alcoholism 
rarely require any treatment per se. The effects of the alcohol pass off 
during the sleep, and although the patitnt shows for some days the 
grind of the mill of the gods, he soon recovers. Should, however, the 
coma be deep, gastric lavage should be employed. If the patient is 
unruly or maniacal, a hypodermic injection of apomorphine (\ grain, 
0.01 gram) usually induces not only nausea and vomiting, but also 
quietude. In the event of convulsions, a few whiffs of chloroform may 
be given, or chloral (20 grains, 1.3 gram) and bromide (40 grains, 
2.6 gram) may be administered, and repeated if necessary in two hours. 
If the patient is much depressed (low temperature, etc.), resort should 
be had to energetic frictions, external heat, enemas of hot saline solu- 
tion and coffee, and coffee by the mouth (or stomach tube), hypodermic 
injections of strychnine and atropine, artificial respiration, the faradic 
current to the respiratory muscles, etc. 

The chronic alcohol habit is best treated in a hospital or similar 
institution where the physician has entire command of the situation. 
The alcohol should be withdrawn as rapidly as possible (three to five 
days); there is neither logic nor advantage in continuing it in gradually 
decreasing amounts for two or three weeks. The following may be given 
as a substitute for the alcohol: 

1$ — Tincture of nux vomica 6 drams 

Tincture of capsicum . 2 drams 

Ammonium bromide 5 drams 

Elixir of ammonium valerianate 2 ounces 

Syrup of ginger 2 ounces 

Water, sufficient to make 8 ounces 

S. — One tablespoonful (15 c.c.) four times a day. 

Atropine hypodermicly, t -|~q grain (0.0005 gram), twice or thrice 
daily, will keep in control the nervousness in the early days of absti- 
nence from the alcohol. An additional dose of a bromide, or chloral 
(20 grains 1.3 gram), or hyoscine (y^- grain, 0.00065 gram), or sul- 
phonal or veronal, etc., may be given at bedtime to induce sleep. Good 
results also attend frequent feedings, perhaps of highly seasoned food, 
for a time at least (to satisfy the craving for something stimulating); 
free catharsis; a daily or twice daily hot bath followed by a cold 
douche; and some outdoor exercise. 

If the alcoholic subject is seen in delirium tremens or at the end of 
a debauch (" threatened with delirium tremens"), the first essential 
is to get him asleep; often he will awake from a prolonged sleep entirely 
refreshed, and the danger has past. He must be kept in bed (preferably 
on a mattress on the floor) and gently restrained; the use of wrist- and 
ankle-straps may be necessary, but forcible personal restraint by nurses 
or attendants increases the delirium and resistance. The patient 
should first be given 5 grains (0.3 gram) of calomel and 10 grains (0.6 
gram) of compound jalap powder dry on the tongue, and then a hypnotic 
—chloral (15 grains, 1 gram) and morphine (J grain, 0.008 gram) are the 
best; these doses may be repeated at the end of an hour if the patient 



25 







8 







20 







60 







60 







50 


0- 


-M 



292 INTOXICATIONS 

is still wakeful and restless, but in the event of a weak heart this should 
be fortified with strychnine and digitalis. To the chloral and morphine 
one may add sodium bromide (40 to 60 grains, 2.6 to 4 grams); or he may 
give hyoscine (y-J-g- g ram > 0.00065 gram), paraldehyde (1 to 2 drams, 
4 to 8 grams), etc. A. Lambert advises: 

]$ — Strychnine sulphate ^ grain 01002 

Hyoscine sulphate . jq-q grain 00065 

Apomorphine hydrochloride y 1 ^ grain 0J006 

The use of atropine (y^-g- to -g 1 ^ grain, 0.00065 to 0.001 gram) twice daily 
has also been attended by good results. 

Hypnotics, such as trional, veronal, and the bromides, usually suffice 
after the first prolonged sleep, but none may be needed. Special atten- 
tion must be given to supporting the patient's strength by the use of 
strychnine (^q- grain, 0.002 gram, every four hours) or nux vomica, and 
by an abundance of nutritious food — preferably liquid and hot (milk, 
broths, eggs), perhaps highly seasoned, for several days. A weak heart 
must be supported on well-known principles. Lambert extols the use of 
the belladonna, xanthoxylum (prickly ash), and hyoscyamus mixture 
mentioned under the opium habit. 



OPIUM HABIT. 

(Morphine Habit; Morphinism; Morphinomonia.) 

Taken, as a rule, in the beginning to alleviate pain or to produce 
sleep, or, as in the East, for reasons similar to those that actuate the 
Occidental to take alcohol, opium or morphine, and to a less extent 
codeine and heroin, gradually create an almost if not quite uncontrol- 
lable craving. The habitues, both the pleasure seekers (morphinists) 
and the pain-racked subjects (morphinomaniacs) may take enormous 
amounts — a half to one ounce of opium, a pint of tincture of opium, 
10 to 30 grains of morphine, etc., daily, and the amount is usually in- 
creased with the passage of time. 

Symptoms. — The opium (or morphine) habitue usually has a pale, 
grayish-ashen countenance, and deep-sunk, dreamy, inexpressive eyes; 
he (or she) is withered, emaciated, and prematurely old-looking, restless, 
and irritable. When not under the influence of the drug the patient is 
likely to be depressed, weak, and inactive. As a rule, the appetite is 
impaired and capricious, digestion deranged, the bowels constipated, 
and sleep poor and unrefreshing. Itching of the skin is not uncommon, 
and there may be oedema, etc. Marked perversion of the moral sense 
is common; the habitue' has no regard for his word, either in statement of 
fact or promises. Neurasthenic and hysterical phenomena are common 
in women. Extraordinary suffering and collapse may follow sudden 
discontinuance of the drug. 

Treatment. — It is worse than useless to attempt treatment outside 
of a hospital or sanatorium where the strictest supervision of the patient 



COCAINE HABIT 293 

is possible; the ordinary morphine habitue usually goes to a hospital 
laden with morphine, and will obtain the drug at all hazards. As a rule, 
the patient should remain in bed for ten days or two weeks. The mor- 
phine should be withdrawn rather rapidly, that is, within a week. At 
the same time the patient should receive a cold tub bath or sponge bath 
in the morning, and a hot bath at night; and massage in the middle of 
the day, or in the afternoon. An abundance of simple nutritious diet 
should be given at short intervals. Much of the abdominal distress, 
and pain, nausea and vomiting, diarrhoea, etc., has been attributed 
to hyperchlorhydria, which may be met by the aforementioned fre- 
quent feedings, large doses of sodium bicarbonate, etc. Restlessness 
and nervousness may be controlled with the bromides, valerian, etc.; 
sleep may be promoted by an occasional dose of sulphonal, veronal, 
chloral, etc., if required, but caution is necessary lest one drug habit 
be substituted for the other. The cardiac and general asthenia may 
require the use of strychnine, aromatic spirit of ammonia, and other 
diffusible stimulants, strophanthus, digitalis, etc. Lambert extols 
the following as a specific in the treatment of drug (morphine, cocaine, 
alcohol) addictions: 

1$ — Tincture of belladonna 2 ounces 60J0 

Fluid extract of xanthoxylum, 

Fluid extract of hyoscyamus of each 1 ounce 30j0 

Lambert advises that the treatment be begun with 4 compound cathartic 
pills and 5 grains of blue mass, and a soapsuds enema. When the pills 
have begun to act, 6 to 8 minims of the belladonna mixture should be 
given every hour, and every six hours the dose should be increased 
2 minims, until 14 to 16 minims is being taken hourly, or the patient 
has shown signs of belladonna intoxication (dilated pupils, dryness of 
the throat, a red rash, rapidity and incisiveness of speech, or beginning 
delirium). Should these develop, they should be allowed to subside, 
whereupon one should begin with the mixture again in 8 minim doses 
hourly. With the first dose of the mixture, from one-half to two-thirds 
of the total daily amount of morphine or cocaine to which the patient 
has become accustomed, is given — in three equal doses at half-hour 
intervals. The bowels must be opened thoroughly — with compound 
cathartic pills, blue mass, calomel, castor oil, etc. At the end of thirty 
hours strychnine, digitalis, or strophanthus should be commenced. The 
treatment is said to take away the desire for morphine, cocaine, or 
alcohol in less than five days, with a minimum of discomfort and 
suffering to the patient. 

COCAINE HABIT. 

(Cocainism.) 

The cocaine habit is usually acquired in consequence of taking the 
drug to relieve exhaustion (sexual, postalcoholic, etc.), or to alleviate 



294 INTOXICATIONS 

pain, neuralgia, chronic nasal catarrh, etc. As much as 30 or 40 grains 
daily may be taken by the mouth or hypodermicly. 

Symptoms. — Cocaine at first produces a feeling of mental exhilaration 
and bodily vigor, freedom from pain and distress, and a subjective 
sense of the ability to accomplish the mind's desires and the heart's 
cravings; but the judgment becomes perverted and accomplishment 
by no means keeps pace with stimulated imagination. In the course 
of time these feelings give way to nervousness, irritability, introspection, 
apprehension, and insomnia. As the use of the drug is persisted in, the 
periods of peace and exhilaration become shorter, and the restlessness, 
depression, and distorted mentality more marked; the appetite fails, 
the patient emaciates, and even insanity may ensue. Some subjects 
exhibit a periodicity in their addiction to the drug; and others are addicted 
also to alcohol, morphine, etc., concurrently or intermittently. 

Treatment. — The treatment in general should follow the principles 
suggested under morphinism. Withdrawal of the cocaine should be 
moderately rapid — within a week, the bromides, valerian, hyoscyamus 
being used to control the nervousness; or one may have recourse to the 
belladonna mixture advised by A. Lambert. Care should be taken 
not to substitute the alcohol, morphine, or chloral habit for the cocaine 
addiction. 

LEAD POISONING. 

( Plumbism ; Sa turnisim. . ) 

Lead poisoning is a common result of one of the so-called dangerous 
industrial trades — lead working. Under like conditions women seem 
to be more susceptible than men. The lead usually enters the system 
by way of the respiratory tract (inhalation of lead-dust-laden atmosphere), 
by way of the digestive system (contaminated food and drink; pro- 
fessional administration of lead), or by way of the skin (cosmetics, 
hair dyes, thread, etc.). Less comnaonly poisoning may follow the 
use of lead douches in the vagina, etc. 

Pathology. — In acute and fatal cases the conspicuous lesion is catarrhal 
gastro-enteritis and softening of the brain. Goadby and Goodbody 
believe that the essential and primary action of lead intoxication is the 
production of minute and microscopic hemorrhages in various portions 
of the body, including the nervous system, and that the clinical symp- 
toms of lead palsy and its good prognosis when treated early are explain- 
able by the presence of minute hemorrhages in the peripheral nerves. 
In advanced cases the lesions are those of multiple neuritis, with atrophy 
and degeneration of the muscles; degenerative lesions may also be 
found in the ganglion cells of the anterior cornua of the spinal cord. 

Symptoms. — Acute Lead Poisoning. — Symptoms may develop after 
a few weeks exposure, or, rarely, they may not come on until after years 
of exposure. The manifestations are usually those of severe gastro- 
intestinal catarrh (nausea, vomiting, colicky pain, diarrhoea or con- 



LEAD POISONING 295 

stipation), which may lead to collapse and death. There may be asso- 
ciated coma or convulsions, cerebral or peripheral paralyses, rapidly 
developing anemia, suppression of urine, albuminuria, slow pulse, etc. 

Chronic Lead Poisoning.— The significant symptoms of chronic 
lead poisoning consist of lead colic, lead paralysis, lead encephalopathy, 
and lead cachexia. 

Lead colic (painters colic) is the most common manifestation. The 
pain, which may be preceded by ill-defined gastro-intestinal disorder, 
is usually very severe, paroxysmal (colicky), and is often diffuse, although 
it may be localized to the region of the umbilicus, the epigastrium, or 
hypogastrium; it is usually relieved by firm pressure. The paroxysms 
may continue for a few moments to an hour or more, and when the 
severe pain subsides more or less dull aching pain continues. Consti- 
pation is the rule, but the paroxysms of pain may be associated with 
diarrhoea. Relapses are common, and exposure may cause chronic 
lead colic. 

Lead paralyses (or palsies) are quite common, and may come on 
suddenly or slowly. They are due to peripheral neuritis, and are asso- 
ciated with tremors, wasting of the muscles, reactions of degeneration, 
paresthesias, neuralgias, arthralgia, etc. The following types have been 
distinguished: (1) The musculospiral type (antibrachial type, wrist- 
drop), in which involvement of the musculospiral nerve leads to paralysis 
of the extensor muscles of the wrist and the fingers (except the supinator 
longus) and the characteristic wrist-drop. In long-continued cases 
slight backward displacement of the corpus and distention of the syno- 
vial bursa? (Griibler's tumor) may occur. (2) The brachial type, in 
which the deltoid, biceps, brachialis anticus, and sometimes also the 
pectoral muscles are involved. (3) The Aran-Duchenne type, common 
in tailors, in which the small muscles of the hand and the thenar and 
hypothenar eminences are involved (resembling chronic anterior polio- 
myelitis). (4) The peroneal type, in which the lateral peroneal and the 
extensor muscles of the toes are involved (steppage gait). Rarely there 
may be paralysis of the laryngeal or intercostal nerves; or a palsy 
resembling Landry's ascending paralysis may occur; or hemiplegia 
may ensue; or the condition may resemble tabes dorsalis. 

Lead encephalopathy may be manifested by mild symptoms such as 
headache, dizziness, excessive irritability or depression, tremor, insomnia, 
dimness of vision, tinnitus aurium, etc., or by severe symptoms, such as 
delirium, coma, or convulsions. The delirium is marked by periods 
of violence and intervals of somnolence, which may be followed by 
true sleep and convalescence. Coma may come on suddenly or grad- 
ually and be preceded or attended by delirium or convulsions. The 
convulsion may be localized or generalized and resemble epilepsy. 

Lead cachexia is characterized by a pallid, sallow complexion, coated 
tongue, a peculiar dry, metallic taste in the mouth, fetid breath, gastro- 
intestinal derangements, constipation perhaps alternating with attacks of 
diarrhoea, malaise, weakness, and emaciation. 



296 INTOXICATIONS 

Examination of the blood reveals a well-marked anemia— oligocythemia 
and oligochromemia (50 per cent, or thereabout), a characteristic baso- 
philic degeneration of the erythrocytes, some erythroblasts, and perhaps 
slight leukocytosis. In most cases there is a bluish or grayish -black 
line (2 to 3 mm. wide) at the margin of the gums, in the papilla? (lead 
sulphide precipitated in the tissue by the sulphuretted hydrogen of the 
tartar); it must be distinguished from a somewhat similar-looking line 
between the gums and the teeth which is readily removed with a tooth- 
brush. The HC1 content of the gastric juice is usually diminished or 
absent, and lactic acid may be present. Arteriosclerosis with hyper- 
trophy of the heart and chronic interstitial nephritis eventually ensue. 

Diagnosis. — The diagnosis is easy in the presence of any of the char- 
acteristic symptoms, but in a case of coma it may be exceedingly difficult. 
The bluish line in the gums and basophilic degeneration of the erythro- 
cytes are of much importance. In other cases the first clue to the diag- 
nosis may be a knowledge of the patient's occupation or of his exposure 
to the poison. In some cases lead may be detected in the urine. 

Prognosis. — The outlook is favorable in all but the severe encephalo- 
pathies, which often result fatally, or if recovered from may eventuate 
in mental deterioration. Wrist-drop if neglected may prove intractable. 

Treatment. — As soon as symptoms become in the slightest degree 
manifest, the patient should be removed from exposure to lead and 
warned against again subjecting himself to it, since there is always 
danger of relapse in susceptible individuals. Workers in lead should 
wear a mask, and should be scrupulously clean, especially in regard to 
the hands (finger nails), which often are the indirect source of intoxi- 
cation (in eating, etc.). In the severe acute poisonings, sodium and 
potassium sulphate should be administered (to precipitate insoluble 
lead sulphate); opium should be given for pain, and stimulants for the 
collapse. Lead colic should be treated by magnesium sulphate, calomel 
and compound jalap powder; morphine and atropine hypodermicly 
for the pain and to relax the intestinal musculature; hot applications 
to the abdomen, etc. Potassium iodide (15 to 30 grains, 1 to 2 grams, 
daily) should be administered to promote elimination of the lead; iron 
should be given for the anemia, and massage, passive motion, exercises, 
and electricity for the local paralysis. 

Carles has proposed the production of a sterile abscess (by the intra- 
muscular injection of 1 c.c. of turpentine) with a view to withdraw 
into the abscess by means of the phagocytes the lead deposited in the 
body; and the later evacuating of the abscess. 



ARSENICAL POISONING. 

Arsenic may enter the system in poisonous amounts by the intestinal 
or the respiratory tracts. Most cases of poisoning are accidental, the 
poisoning being acquired in the pursuit of certain dangerous trades, 



MERCURIAL POISONING 297 

such as the manufacture of colored wallpapers, various fabrics, artificial 
flowers, etc., but poisoning may also follow the criminal administration 
or taking of Rough-on-rats, Paris green, etc. ; occasionally it follows the 
therapeutic administration of arsenic. 

Symptoms. — Beginning therapeutic overaction or intolerance of 
arsenic is manifest by salivation, epigastric pain and distress, nausea, 
vomiting, diarrhoea and tenesmus, oedema and itching of the eyelids, 
urticaria, pityriasis, psoriasis, eczema, muscular tremors, and contrac- 
tions and stiffness of the joints. In what may be called acute poisoning 
the gastro-intestinal symptoms are aggravated, the urine and the 
feces may be bloody, and there may be anuria. In some cases gastro- 
intestinal symptoms are in abeyance and symptoms resembling opium 
narcosis may come on; later numbness, sharp darting pains, or paral- 
yses may supervene. In chronic arsenical poisoning, the symptoms, 
which may develop insidiously, are usually those of increasing anemia 
and debility, pigmentation (also keratosis or herpes) of the skin, and 
multiple neuritis (paresthesia, neuralgia, paralyses), involving the 
legs (extensor and peroneal muscles) rather than the arms, and usually 
associated with rapid and marked atrophy of the muscles. There may 
be also divers gastro-intestinal disturbances, redness and bleeding of 
the gums, stiff joints, etc.; pseudotabes may ensue. 

Diagnosis. — The diagnosis may be based upon known exposure to the 
influence of the poison, pigmentation and other lesions of the skin, 
multiple neuritis, and the detection of arsenic in the urine. 

Treatment. — The treatment consists in avoidance of the source of 
intoxication; potassium iodide to promote elimination; iron for the 
anemia; and massage, electricity, etc., for the neuritis. 

MERCURIAL POISONING. 

(Hydrargyrism ; Mercuria lism. ) 

Mercury is extensively used in the manufacture of mirrors, bronzes, 
thermometers, decorative novelties, cosmetics, etc., so that poisoning 
not infrequently ensues. The poison may gain access to the system 
by way of the alimentary tract, the respiratory tract, or the skin. The 
therapeutic administration of mercury (calomel, blue mass, etc.) also 
may lead to poisoning. 

Symptoms. — The acute symptoms consist of fetid breath, a metallic 
taste in the mouth, salivation, swelling, sponginess, and frequently 
hemorrhage of the gums, sometimes even loosening and shedding of the 
teeth, with ulceration and necrosis of the jaw. The characteristic of 
the chronic cases is muscular tremor (trembles), which at first occurs 
only on movement or excitement, but later becomes more or less con- 
tinuous, usually first involving the tongue and face (interfering with 
speaking) and later the extremities (interfering with arm movements 
and walking). Physical strength lessens and mental deterioration may 
ensue. 



298 INTOXICATIONS 

Diagnosis. — The symptoms and the history are usually conclusive. 
Multiple sclerosis, paralysis agitans, and other disorders associated 
with tremors should be readily excluded. 

Treatment. — The avoidance of the poison is the first essential of the 
treatment. Potassium iodide should be given to promote elimination. 
A gargle of tannic acid and antiseptics may be used during salivation. 
Iron, quinine, and strychnine in tonic doses should be given. 



SNAKE-VENOM POISONING. 

The common poisonous snakes of the United States are the Crotalus 
(rattlesnake), the Ancistrodon (water moccasin and copperhead), and 
the Elaps (coral and harlequin snake) ; in Europe only the vipers abound ; 
in Asia, the cobra, vipers, crotalus, elaps, and other poisonous varieties 
are found. The venom is contained in a gland with a maxillary fang 
that becomes unsheathed in activity; the venom is viscid, and varies in 
color from pale amber to deep yellow. Noguchi states that snake venom 
owes its toxicity to the presence of several active principles, which are 
present in varying proportions in different venoms, whence the dif- 
ferences in their activity. These toxic principles are: That which pro- 
duces instantaneous intravascular clotting of the blood; that which 
attacks the nervous system (neurotoxin); that which causes rupture 
of the walls of the capillary vessels and extensive hemorrhages (hemor- 
rhagic principle); that which attacks the blood corpuscles, causing 
hemolysis and agglutination (hemolytic and hemo-agglutinative prin- 
ciples); those which cause lysis of other body cells (cytolytic principles); 
those which protect or harden the erythrocytes; and that which causes 
a loss of the bactericidal property of the blood. 

Symptoms. — Noguchi states that the symptoms observed in man may 
be divided into local and general. The local symptoms consist in a 
rapidly appearing, inflammatory swelling at the site of the bite, followed 
by more or less ecchymosis and necrosis, with or without pain, and 
often with the appearance of lymphangitis and local phlegmon. The 
constitutional symptoms are fever, cerebral and spinal disturbances, 
especially of the medulla, including paralysis of the respiratory centre, 
and rapid advance of motor paralysis. Hematuria, hemoglobinuria, 
hematemesis, diarrhoea, vomiting, amaurosis, headache, vertigo, violent 
dyspnoea, and general convulsions are often observed. In viperine 
poisoning there may be also cold perspiration and a small intermittent 
pulse. Death may ensue in two minutes (Crotalus poisoning), more 
commonly after about fifteen minutes; or it may be delayed for from 
twelve to forty-eight hours, or longer. 

Treatment. — An attempt should be made to retard the absorption 
of the venom, by the application of a ligature about the region of 
the bite, by opening the wound and cupping or sucking, or otherwise 
mechanically removing the venom. One should also inject into and 



FOOD POISONING 299 

around the bitten region potassium permanganate (1 per cent.), calcium 
chloride (1.5 per cent.), chromic acid (1 per cent.), or ammonia. Alcohol, 
coffee, and tea may be used, as well as oxygen inhalations, and saline 
intravenous injections. Noguchi states that experimentally strychnine, 
morphine, nicotine, and curare are not only of no value, but distinctly 
harmful. The specific treatment is Calmette's antivenin, which 
should be used immediately if it is available. Unfortunately each 
venom seems to require for neutralization a specific antivenin; an 
efficient polyvalent antivenin has not yet been prepared. 

FOOD POISONING. 

{Ptomaine Poisoning; Bromatotoxism.) 

Poisoning may follow the eating of food or pseudo-food: (1) Because 
the substance taken is in itself poisonous, that is, it contains an en- 
dogenous poison, and, speaking strictly, can not, therefore, be called 
a food (certain mushrooms, fish, etc.); or (2) because to an otherwise 
suitable food an exogenous poison may be added. In addition, some 
persons are unusually susceptible to the influence of, and become more 
or less ill from eating, certain foods, toward which mankind reacts 
in what may be called a standard manner, such as strawberries, buck- 
wheat, veal, liver, etc. The exogenous poisons found in foods may be: 

(1) Various chemical adulterants added to preserve the food or to mask 
putrefactive processes, such as various sulphites, salicylic acid, boric 
acid, benzoic acid (and their salts), formaldehyde, potassium nitrate, 
etc.; or coloring matters, such as salts of copper, lead, arsenic, etc. 

(2) Metals, such as tin, lead, copper, etc., derived from vessels con- 
taining food. (3) Divers sorts of microorganisms — bacteria, fungi, 
and zooparasites of specific infections, as well as the organisms of 
putrefaction. The alkaloidal products of putrefaction are spoken of 
as ptomaines, and their ill effects as ptomaine poisoning. 

Meat Poisoning (Kreatoxism). — Meat poisoning may result from eating- 
meat (especially sausage, ham, and pork, but also beef, veal, game, and 
all kinds of corned meat) infected with Bacillus botulinus (so-called 
botulism), Bacillus enteritidis (Gartner), Proteus vulgaris, Bacillus 
coli, Bacillus paratyphosus, etc. The nature of the poison (kreatoxicon) 
has not been determined. The symptoms may be gastro-intestinal 
or nervous (toxemic), or both. Often there is a period of incubation of 
several hours or more, in which there may be no symptoms. The 
onset is often sudden, with abdominal pain, nausea, vomiting, diarrhoea, 
headache, weakness, and neuromuscular pains; there may be an initial 
chill or chilliness and subsequent fever (101° to 103°); headache, vertigo, 
faintness, and profuse sweating are common. In some severe cases 
the diarrhoea is profuse and quite exhausting (choleraic form), and with 
the toxemia may lead to collapse and death. 

Milk Poisoning (Galactotoxism) and Cheese Poisoning (Tyrotoxism).— 
Poisoning may ensue from the use of milk and its derivatives (cheese, 



300 INTOXICATIONS 

ice-cream, etc.), the toxic agents being tyrotoxicon (Vaughan) and per- 
haps other ptomaines. In some cases the colon bacillus has been found 
in the milk. The symptoms consist of nausea, vomiting, diarrhoea, with 
perhaps bloody or cholera-like discharges, neuromuscular pains and 
cramps in the legs, fever, and collapse. There may be a rash resem- 
bling that provoked by belladonna. 

Fish Poisoning (Ichthyotoxism) and Shellfish Poisoning (Mytilotoxism).— 
Fish poisoning may follow the eating of fish that has undergone putre- 
faction, or of certain parts (roe, testicles, poison glands connected with 
the fins, etc.) of otherwise wholesome fish. The symptoms may be 
gastro-intestinal (pain, nausea, vomiting, and diarrhoea), or nervous, 
with collapse, or they may resemble those of belladonna poisoning 
(dryness and constriction of the throat, dilatation of the pupils, ptosis, 
delirium, convulsions, coma). Shell -fish poisoning may follow the eating 
of unwholesome mussels, oysters, lobsters, crabs, etc. A poisonous 
principle (mytilotoxin) has been isolated in certain cases. The symp- 
toms are largely gastro-intestinal (pain, nausea, vomiting, and diar- 
rhoea), with which a rash and other symptoms suggesting belladonna 
poisoning are often added. The pulse may become rapid and the 
patient collapsed, or he may pass into coma. 

Grain Poisoning (Sitotoxism). — Ergotism. — Ergotism results from 
eating rye and other grain infected with Claviceps purpurea (the ergot 
fungus). Kobert has isolated three poisonous substances — sphacelinic 
acid, cornutin, and ergotinin; to these Jacoby has added sphacelotoxin, 
which he believes to be the specific poison. The symptoms may be 
acute or chronic. The acute symptoms are largely gastro-intestinal with 
collapse. The chronic disorder may be of the gangrenous or the con- 
vulsive type. The gangrenous type is characterized by pain, paresthesias, 
anesthesias, blood stasis, and gangrene of the fingers, toes, nose, ears, etc. 
The convulsive type is characterized by a prodromal period of from 
ten to fourteen days, during which there may be pains and paresthesias, 
and perhaps fever; these are followed by muscular spasms and contrac- 
tures, especially of the arms and legs, that may last for a few hours or 
days and recur. Delirium and convulsions may supervene. Eventually 
a pseudotabes (posterior spinal sclerosis) ensues. 

Lathyrism (Lupinosis). — Lathyrism results from eating meal 
(and bread) to which vetch seed (Lathyrus sativus and Lathyrus cicera) 
has been added, usually as a substitute for wheat. It occurs in Italy, 
Austria, Africa, and India. The nature of the poison is not known. 
The chief symptoms consist of paresthesias, spastic paraphlegia (involv- 
ing the legs), increased reflexes, etc. 

Pellagra (Maidism). — Pellagra results from eating corn (maize) 
that has become in some unknown way unwholesome or spoiled. It 
is common in Italy, France, Spain and in the southern and western 
parts of the United States. The symptoms develop insidiously, the 
earliest manifestations usually being gastro-intestinal — anorexia, stoma- 
titis, salivation, epigastric pain or distress, diarrhoea, and a gradually 



FOOD POISONING 301 

increasing anemia, asthenia, disinclination to exertion, and psychic 
depression. The fully developed disease is characterized by cutaneous, 
digestive, and nervous symptoms. There is at first a characteristic 
pellagrous erythema that usually comes on first in the spring, tends to 
subside and recur (in the fall and spring). It develops bilaterally 
especially on the exposed surfaces, the hands, arms, face, and neck; that 
is, it seems to be related to the action of the actinic rays of the sun; it 
may be dry (usually early) or wet; the lesions become pigmented (liver- 
yellow or chocolate color) and usually progress to desquamation, exfolia- 
tion, and gangrene of the skin, which are followed by cicatrization. 
The characteristic digestive symptoms consist of stomatitis, the cardinal- 
red tongue (Watson), the bald tongue (Sandwith), or the stippled, bluish- 
black tongue (Lavender) ; salivation, pyrosis, and diarrhoea (fetid, slimy, 
greenish stools), sometimes bloody stools, may occur. The nervous 
symptoms consist of neuromuscluar pains in the back and legs, spinal 
tenderness, headache, vertigo, unilateral or bilateral mydriasis, muscular 
spasms, exaggerated reflexes, later paralysis with lessened or absent 
reflexes, mental depression, delusions, hallucinations, melancholia, and 
insanity. Mild cases may be afebrile, but fever (102° to 105° or more) 
is not uncommon. Improvement may occur after the lapse of several 
months, but recurrences especially in the fall and spring are common. 

Vegetable Poisoning. — Poisonous symptoms sometimes follow the 
eating of potatoes that have "sprouted." The symptoms are attributed 
to solanin, which, under the influence of Bacillus solaniferum, increases 
from the normal 0.06 per cent, to as much as 0.4 per cent. The symp- 
toms consist of digestive disturbances (pain, nausea, vomiting, diarrhcea), 
jaundice, headache, chills, fever, and prostration. 

Treatment. — The treatment of food poisonings consists primarily 
in avoiding the source of the intoxication, the proper preservation of 
food, careful agricultural supervision to avoid contamination of grain, 
etc., and in the cases of pellagra, etc., removal from the region of endemic 
intoxication. In the acute ptomaine poisonings the stomach should be 
washed out, and the bowels thoroughly evacuated by a brisk cathartic; 
following this the diarrhcea should be controlled by bismuth, lead, 
opium, etc. Stimulants, such as alcohol and strychnine, are often 
required. Hypodermoclysis and enteroclysis also may prove useful 
in reviving a prostrated patient and favoring elimination of the pto- 
maines. Arsenic and quinine have proved of value in pellagra; tonics 
also are indicated. Recently, Cole and Winthrop have recommended 
the transfusion of pellagrinous blood (believed to contain antibodies), 
or, if this be not obtainable, of normal blood. 



SECTION III. 
DISORDERS OF METABOLISM. 



Pathological Physiology. — The disturbances of metabolism to which 
the body is subject are many and various. Some of these constitute 
clinical entities and are discussed under appropriate headings, such as 
diabetes, gout, obesity, etc. ; others in a broad sense include many of the 
disorders of the ductless glands and of internal secretion, which also are 
discussed under appropriate headings ; others are not so well defined nor 
so well understood. These have not attained the dignity of clinical enti- 
ties, being, as a rule, merely more or less obtrusive manifestations of a 
wide variety of diseased conditions; they are alike, however, in that they 
lead ultimately to more or less pronounced poisoning of the body, and 
since the toxic agent is elaborated within the body, they are distinguished 
as endogenous poisonings or auto-intoxications. In the majority of cases 
the poisonous agent has not been identified with certainty, so that these 
auto-intoxications are still the subject of more speculation than of dem- 
onstrated fact. Nevertheless, three types of auto-intoxications may be 
distinguished, although they are not sharply delimitable the one from 
the other nor from other diseased states, of which often they are merely 
a manifestation: (1) Gastro-intestinal auto-intoxications; (2) acidosis 
and acid intoxications; and (3) retention auto-intoxications. 

Gastro-intestinal Auto-intoxications. — Gastro-intestinal auto- 
intoxications conceivably may result from the absorption of: (1) Poisonous 
intermediate products of digestion; (2) poisonous end products of meta- 
bolism that normally are detoxified in the body or excreted therefrom ; 
and (3) certain products of putrefaction. It is difficult, if not impossible 
to separate these from the results of the activity of bacteria — those 
normal in the intestine as well as those foreign thereto, since it is not 
improbable that bacterial activity, of much importance in the orderly 
performance of some of the intestinal functions, if perverted, may injuri- 
ously affect the intestinal enzymes. Abeyance of the detoxifying func- 
tion of the liver is often, at least in part, answerable for the gastro- 
intestinal auto-intoxications. The evidence that intermediate and end 
products of digestion, such as peptones, purins, nucleo-proteins, etc., 
may be absorbed and give rise to toxic symptoms is very unsatisfactory 
and inconclusive, and for the present may be disregarded. Putrefactive 
changes in the intestine involve almost solely the aromatic and sulpl 



uir 



304 DISORDERS OF METABOLISM 

groups of the protein molecule. The aromatic bodies yield indol, phe- 
nol, and skatol, which uniting with sulphuric acid, may appear in the 
urine (indoxyl-sulphate, so-called indicanuria, etc.). This occurs in the 
event of protein decomposition elsewhere than in the intestine, and it is 
doubtful whether of itself it gives rise to symptoms; but with reserve it 
may be interpreted as a measure of intestinal putrefaction: it occurs 
most rapidly and in greatest amount in obstruction or paralysis of the 
small intestine. Various other disorders are attributed, with more or 
less reason, to gastro-intestinal intoxication: senescence and ultimately 
death (MetchnikofT) ; the headache and general malaise of chronic con- 
stipation; chlorosis (Sir Andrew Clark); pernicious anemia, attributed 
by William Hunter to oral and gastro-intestinal toxemia; tetany, some- 
times associated with gastric dilatation, and due apparently at least 
indirectly to the absorption of a poison from the stomach; the toxemia 
and death of high intestinal obstruction (duodenal auto-intoxication, 
disturbance of the balance of physiological intra-enteric enzymotic bal- 
ance, Maury); cirrhosis of the liver; chronic disease of the joints; a 
so-called intestinal infantilism, described by Herter and attributed by 
him to chronic intestinal infection due to the overgrowth and persistence 
of the bacterial flora of the intestine belonging normally to the nursling 
period; and a rare form of cyanosis, known as enterogenous cyanosis, 
due in the one series of cases to methemoglobinemia, the result of the 
absorption of nitrites from the intestine in chronic diarrhoea, and amen- 
able to a milk diet, and due in another series of cases to sulph-hemoglo- 
binemia, the result apparently of putrefaction of the proteins in chronic 
constipation, and amenable to treatment directed toward the constipa- 
tion. The treatment of these gastro-intestinal auto-intoxications com- 
prises attention to any demonstrable focus of intoxication, such as 
pyorrhoea alveolaris or other form of oral sepsis, chronic ulceration of 
the bowel, rectum, etc. ; regulation of the diet, especially restricting the 
amount of meat, and giving in the one case milk, as well as milk soured 
with the lactic acid bacillus (Bacillus bulgarius) ; in another case food 
that leaves sufficient residue to promote free evacuation of the bowels; 
medicinal and other treatment of constipation, if it be present; the 
use of so-called intestinal antiseptics, such as salol, /?-naphthol, bismuth 
sulphocarbolate, resorcin, etc. ; and high colonic irrigations 

Acidosis and Acid Intoxications. — Acidosis is a diseased condition 
in which organic acids, notably /3-oxybutyric acid, diacetic acid, and 
acetone (the so-called acetone bodies) appear in abnormal amounts in 
the blood and the urine (ketonuria) ; acid intoxication is a diseased con- 
dition in which in addition toxic symptoms develop. There is still some 
discussion as to whether these acetone bodies are toxic per se, or whether 
they exert their deleterious action merely because they are acid, robbing 
the body of native alkali, diminishing the power of the blood to take up 
carbon dioxide, and leading to tissue asphyxiation; perhaps both factors 
are operative in human pathology. These acetone bodies are derived 
largely, if not exclusively, from the lower fatty acids; perhaps in small 



DIABETES 305 

part from the fatty acid moiety in protein, such as leucin. The condi- 
tion of acid intoxication may be the result of an augmented formation 
of these acetone bodies, or of a deficiency of bases; and it is found in: 
(1) Diabetes, of which it forms a conspicuous and serious feature, and 
under which heading it is discussed; (2) starvation of whatsoever sort: 
insufficiency of food; inability to take or utilize food, as in stricture or 
carcinoma of the oesophagus, stomach, or intestine; diseased conditions 
of the gastro-intestinal tract leading to long-continued rectal feeding, 
etc.; it is especially likely to supervene if oxidation is deficient and 
little or no carbohydrate is taken; (3) the febrile state, in which in 
addition to destruction of the body fat and protein, the supply of food 
is often insufficient and cannot be properly metabolized; (4) certain 
ill-understood conditions of the gastro-intestinal tract, usually associated 
with constipation, in which I have seen it present in high grade; (5) 
after anesthesia; (6) in young children, and in excessive degree in the 
recurrent vomiting of unknown cause in children; and (7) in some cases 
of pernicious vomiting of pregnancy. The treatment of the acidosis con- 
sists, in brief, in preventing, if possible, the formation of the acetone 
bodies by a judicious combination of fat, protein, and carbohydrate 
(discussed under diabetes), by neutralizing the circulating acids (by 
administering large amounts of sodium bicarbonate or other alkali), 
and by supplying deficient bases, such as calcium and magnesium. 

Retention Atjto-intoxications. — To the retention of excrementi- 
tious products, auto-intoxications, such as uremia, puerperal eclampsia, 
and so-called cholemia are often attributed; but the nature of the sup- 
posed excrementitious products have not been determined, and there is 
considerable evidence tending to support the view that in these condi- 
tions the detoxifying function of the liver is the major factor at fault: 
the complete elucidation of the many problems herewith concerned must 
await future investigations. Asphyxia may be looked upon as a form 
of auto-intoxication due to the retention of carbon dioxide. The 
toxemia that follows extensive burns may be due to the retention of 
toxic substances incapable of elimination by the burned skin, or to the 
absorption of a toxic substance from the burned areas. Retention of 
sodium chloride is at least one factor in the production of the oedema 
of nephritis, and perhaps of other cedemas. 



DIABETES. 

{Diabetes Mellitus.) 

Diabetes is a disorder of metabolism, involving chiefly the carbohy- 
drates, and characterized clinically by hyperglycemia, glycosuria, and 
ultimately ketonuria and acid intoxication. 

Etiology.— Diabetes occurs at all ages, but is most common after the 
fortieth year; almost one-third of the cases develop in the sixth decade, 
and about one-fifth prior to the thirtieth year; but it may develop in 
20 



306 DISORDERS OF METABOLISM 

advanced life as well as in infancy. It is more common in males than in 
females in the proportion of 3 to 2. In general, it is less common in 
this country (though increasing) than it is in Europe; it is especially 
common among Hebrews, and comparatively rare among negroes. It 
is a disease of the well-to-do, rather than of the poor (in the proportion 
of 10 to 1, von Noorden). Hereditary influences are active in some cases, 
diabetes itself, gout, obesity, and neuropathies being common in the 
antecedents, as well as in the immediate family of diabetic subjects. 
It is not uncommon in husband and wife (conjugal diabetes), which 
without much reason has suggested an infectious cause to some 
observers. 

The direct cause of diabetes is not known. An unhygienic mode of 
life, exposure to wet and cold, overeating, excessive indulgence in car- 
bohydrates and in meat, alcoholism, sedentary habits, prolonged anxiety, 
mental strain, emotional and other nervous disturbances, etc., have 
been credited with etiological significance. The combination of seden- 
tary habits, excessive eating (carbohydrates and meats) and drinking 
(alcoholism), and prolonged mental strain (absorption in business 
pursuits, large, financial, and other responsibilities) is common in those 
who develop diabetes. Disorders that are sometimes attended by tem- 
porary glycosuria seem sometimes also to lead to true diabetes, such 
as: pregnancy; infections (diphtheria, scarlatina, malaria, influenza, 
syphilis, etc.) which perhaps act by setting up pancreatitis; injury and 
disease of the brain and spinal cord (epilepsy, chorea, organic disease 
especially, but not alone, of the medulla and the floor of the fourth 
ventricle), etc. 

Pathology. — The important lesions occur in the pancreas — for our 
knowledge of which fact we are indebted to Minkowski, von Mering, 
Opie, etc. Cecil recently, studying 90 cases, found lesions of the pan- 
creas in 79 (87.4 per cent.); in these the islands of Langerhans were 
always, sometimes alone, diseased (sclerosis, hyaline degeneration, leuko- 
cytic infiltration, and hypertrophy). 97 per cent, of the cases occurring 
after the age of thirty years were associated with lesions of the pan- 
creas, and 87 per cent, occurred in association with chronic inter- 
acinous pancreatitis accompanying arteriosclerosis. 50 per cent, of the 
cases occurring before the age of thirty years were associated with lesions 
of the pancreas; and 75 per cent, of all cases of diabetes in which the 
pancreas was normal occurred before the age of thirty years. In 
addition to disease of the pancreas, the liver is usually enlarged; fatty 
changes are common; there may be cirrhosis, which is usually associated 
with pigmentation of the liver, pancreas, skin, etc. (hemochromatosis, 
bronzed diabetes). The nervous system shows divers but inconstant 
lesions: sclerosis, cysts, or tumors in the medulla and sometimes else- 
where; meningitis and the lesions of different organic diseases; degenera- 
tion of the posterior columns of the cord and peripheral neuritis (the 
cause of so-called diabetic tabes), etc. Usually there is arteriosclerosis 
and hypertrophy of the heart. Hyperglycemia (as much as 0.5 per cent. 



DIABETES 307 

instead of the normal 0.1 to 0.15) is constant, and the opsonic index is 
reduced. The thyroid, pituitary, and adrenals are sometimes enlarged 
or otherwise diseased. Tuberculosis, especially of the lungs, broncho- 
pneumonia, croupous pneumonia, chronic nephritis, gangrene, pyococcic 
infections, such as furuncles, carbuncles, etc., are common complica- 
tions, and may be the cause of the fatal issue. Chronic nephritis 
occurs in about one-half of the cases, and is attributable to the 
polyuria and ketonuria. 

The ultimate nature of diabetes is not yet perfectly understood, largely 
because the fate of carbohydrates in the body in health has not been 
fully elucidated. It is known that normally the carbohydrates of the food 
are converted into glycogen and warehoused in the liver and the muscles; 
and that under some circumstances glycogen may be formed from the 
non-nitrogenous moiety of the food protein as well as the body protein. 
As required by the body for heat and energy, the glycogen undergoes 
destruction, being converted largely into alcohol and carbon dioxide. 
How this glycolysis is effected is still the subject of study. The tendency 
of modern studies is to minimize the significance of the liver, which is 
believed to act chiefly as a storehouse, liberating the stored glycogen 
as it is required and preventing an excess going over into the circulation 
at any one time (which would result in hyperglycemia). There is, 
however, an intimate relationship between the pancreas and the muscles. 
The islands of Langerhans in the pancreas produce a secretion con- 
taining a ferment or zymogen, which, reaching the muscles by way of 
the blood stream, encounters there another ferment or proferment; 
an interaction occurring between the two results in the production of an- 
other ferment, which has the specific property of destroying dextrose 
(glucose). In pancreatic diabetes the pancreatic ferment or zymogen 
is deficient or absent; the muscular ferment or zymogen is not acti- 
vated, the glycolytic ferment is not formed, and glucose is not combusted, 
but passes over in the blood in excess (hyperglycemia), and is excreted 
in the urine (glycosuria). By some investigators it is believed that the 
pancreas, rather than supplying a substance requisite for the proper 
metabolism of sugar, has the property of neutralizing a poison which, 
not detoxified, leads to the accumulation of sugar in the blood. In many 
cases the ability properly to utilize fats also is more or less impaired, and 
/?-oxybutyric acid and its derivatives (oxidation products), diacetic acid 
and acetone, intermediary products of fat metabolism (derivatives of the 
lower fatty acids), are excreted in the urine (ketonuria), and acetone 
also with the expired air. This occurs especially in conditions of carbo- 
hydrate starvation; and, often in the early stages of the disease, at least, 
can be prevented by feeding carbohydrates, which are concerned in pro- 
viding the oxygen necessary for the ultimate oxidation of the fatty acids 
to carbon dioxide and water; later, however, this becomes impossible, 
and a dangerous acid intoxication ensues and may lead to a fatal 
termination. 

Associated disturbance in the carbohydrate and fat metabolism is 



308 DISORDERS OF METABOLISM 

found in some cases of diabetes in the obese, in some of which the 
conversion of carbohydrates into fat is not seriously disturbed, although 
the carbohydrate tolerance may be low (alimentary glycosuria, latent 
diabetes) ; in some of these true diabetes may subsequently develop. Dis- 
order of the protein metabolism is apparent in the fact that an excess of 
protein increases the glycosuria in some cases; some observers believe 
that an excess of protein is at least partly responsible for the disease 
(said to stimulate the thyroid). 

There is in diabetes some relationship between the pancreas and the 
ductless glands — the thyroid, the adrenals, and the pituitary body. 
These, particularly the thyroid and the pituitary, may be found enlarged ; 
and diabetes clinically is found associated with more or less well-developed 
Graves' disease and akromegaly. There is believed to be an antagonism 
between the pancreas and the thyroid; hyperactivity of the thyroid 
may produce glycosuria. It has been found also that the injection of 
adrenalin results in hyperglycemia and glycosuria (adrenal diabetes), 
and an adrenal influence in human diabetes has been postulated (inter- 
ference with the oxidizing power of the pancreas, or an action upon the 
sympathetic nervous system, resulting in the non-warehousing or the 
release of glycogen, with ensuing hyperglycemia and glycosuria). The 
administration of phloridzin (a glucoside) also results in glycosuria 
without hyperglycemia; it is attributed to a toxic influence on the renal 
epithelium, and is used as a test of the functional capacity of the kidney. 
The influence exerted by the nervous system in some cases is not well 
understood. Some observers believe that the disturbance in diabetes 
is not so much in the pancreas and its internal secretion as in the nerves 
that pass through the pancreas; others believe that the nervous influ- 
ence results in the imperfect storage or liberation of glycogen in the 
body. Hyperglycemia is a constant feature— an increase in the sugar 
content of the blood from the normal 0.1 to 0.15 per cent, to 0.3 or 0.5 
per cent. To it is attributable indirectly the fatigue and emaciation, 
on account of the calories thus lost. A daily excretion of 100 grams of 
sugar, representing 400 calories (16 per cent, of the calories required for 
a man weighing 70 kilograms), must be met by increased protein and 
fats, whence the hyperglycemia indirectly results in increased appetite. 

Symptoms. — In the great majority of cases the onset is insidious and 
the disease often has made considerable progress by the time obtrusive 
symptoms become manifest — chronic cases, which may last for years and 
are especially common in subjects past middle life; rarely the onset is 
abrupt, or the disorder, having been existent though ill-declared for some 
time, suddenly (perhaps following an injury, shock, or some emotional 
disturbance) becomes very acute and rapidly progressive — acute cases, 
which are especially common in young subjects and may soon lead to 
death. There is, however, no essential difference between the two 
classes of cases. As a rule, the early symptoms consist of malaise, 
readily induced languor, or loss of flesh and strength; or frequent micturi- 
tion, polyuria, or excessive thirst attracts attention. The fully developed 



DIABETES 309 

disease is characterized by hyperglycemia, polyuria, glycosuria, and 
ultimately ketonuria, acid intoxication, and fatal coma; polydypsia 
and polyphagia; often but not always marked emaciation; and a number 
of variable and inconstant symptoms referable to the different systems 
of organs (complications). 

Major interest and significance attaches to the urine — which is in- 
creased in amount, pale in color, acid in reaction, of increased specific 
gravity, and contains sugar, and often one or more of the acetone bodies. 
The total twenty-four-hour amount of urine averages between three and 
six liters; but enormous amounts (twenty to thirty or more liters) may 
be excreted, and in other cases the amount may be scarcely, if at all, 
above the normal (mild cases; cases markedly improved; under the in- 
fluence of infectious processes; prior to the fatal issue). The specific 
gravity varies, as a rule, between 1025 and 1040, but it is sometimes 
quite low (1015 or less), and rarely it may be very high (1050 to 1070). 
The sugar content varies — from 0.5 to 2 or 3 per cent, in mild cases, to 
5 to 10 per cent, in severe cases. The total amount of sugar excreted 
daily varies from 50 to 200 grams or thereabout in mild cases to 500 
to 1000 grams or more in severe cases; but it is markedly influenced by 
the diet, the mode of life, the form of treatment, and approaching 
fatality and coma. 

The total nitrogen of the urine (normally 10 to 15 grams daily) is 
usually increased (15 to 20 grams or more) ; this is due, as a rule, to the 
increased protein ingestion, but in severe cases, especially with high 
glycosuria and during coma, it is due also to destruction of the body 
protein. The total urea is increased (for the reasons just mentioned); 
the percentage of urea is usually unchanged in the absence of acidosis; 
it is diminished when acidosis is present (on account of the increased 
ammonia) . The creatinin may be increased ; the uric acid may be normal 
or increased. Of special importance and significance is the increased 
output of ammonia. Normally this varies from 0.5 to 1 gram daily, up 
to 1.5 grams on a meat diet; in diabetes it is often increased to 3 to G 
grams, and may reach 8 to 10 grams or more; and instead of forming 2 to 
5 per cent, of the total nitrogen, it may form 10 to 20 per cent. This 
increase is to be interpreted as an effort on the part of nature to neutralize 
the existing acidosis — the result of the acid derivatives of the proteins and 
the fats. The sulphur and phosphorus of the proteins normally are 
oxidized to H 2 S0 4 and P 2 5 , but encountering sufficient fixed bases they 
are neutralized; when in excess, however, they unite with some of the 
ammonia (a product also of protein katabolism) and are carried off 
in the urine. In addition, the acetone bodies, when present, are also, 
at least in part, neutralized by ammonia. The ammonia excretion 
thus is a trustworthy indication of the degree of existing acidosis, and is 
more readily determined. The acetone bodies, /?-oxybutyric acid, dia- 
cetic acid, and acetone (of which the succeeding is the oxidation product 
of the preceding) are often present in the urine (ketonuria) in variable 
amounts. Normally acetone is present in the urine (0.01 to 0.03 grain 



310 DISORDERS OF METABOLISM 

in the twenty-four hours); in diabetes this may be increased to 2 or 
more grams, and the total excretion of acetone and diacetic acid may 
reach 5 to 8 grams, while that of /?-oxybutyric acid may reach 50 to 70 
grams. The acetone bodies are derived from the lower fatty acids of 
the organism and the food, but they occur in the urine only in the event 
of disordered carbohydrate metabolism, the katabolism of 80 to 100 grams 
of carbohydrates being ordinarily sufficient to prevent the ketonuria. 
This rather than the glycosuria is the important index of the severity 
of the diabetes: the acetone bodies are absent in mild cases for a long 
time, and acetone is the first to appear; later, diacetic acid is added, 
and in advanced and severe cases (absolute loss of carbohydrate toler- 
ance, with the excretion in the urine not only of all the ingested carbo- 
hydrates, but also of sugar derived from the non-nitrogenous portion of 
the proteins), all three bodies may be encountered. 

Albuminuria is encountered sometime in at least one-half of the cases. 
It is usually slight in grade, and may be due to local catarrhal disorders 
of the urinary tract, general infections, arteriosclerosis, degeneration of 
the renal epithelium (overwork, from long-continued polyuria, glycosuria, 
and ketonuria) ; in some cases there may be also casts and other evidences 
of true nephritis. Albuminuria, previously absent, is likely to appear 
as a more or less immediate forerunner of coma; indeed, it is not un- 
likely that some of the cases of coma are uremic rather than diabetic 
in nature. 

Most of the other important symptoms are referable to the digestive 
tract and the nervous system. Thirst may be the first obtrusive symp- 
tom, and is often exceedingly distressing; it is probably due to the systemic 
demands for fluids; the intake is usually in direct ratio to the output. 
The appetite may or may not be inordinate. Despite the large amount of 
food taken, digestion is often good, although indigestion (sometimes 
associated with gastrectasia) and constipation (sometimes alternating 
with attacks of diarrhoea) are not uncommon. Despite the large amount 
of food taken the patient may emaciate rapidly. The tongue is usually 
dry, red, and glazed, perhaps fissured; the saliva is scanty; there may be 
aphthous and other forms of stomatitis; and the teeth readily decay. 
The liver may be enlarged — in ordinary diabetes, as well as in bronzed 
diabetes (hemochromatosis). 

Of the nervous symptoms, pruritus, especially of the genitalia, is 
often exceedingly distressing. In addition there may be paresthesias, 
neuralgias, or peripheral neuritis (single or multiple). Bilateral sciatica 
is common. In almost one-half the cases the knee-jerks are diminished 
or lost; this may be associated with paresthesias, irregular pains, and 
neuromuscular cramps in the legs. Some of these cases present a char- 
acteristic steppage gait, degeneration of the posterior columns of the 
spinal cord, perhaps optic atrophy, and other evidence of tabes (so-called 
diabetic tabes). The cranial nerves (especially the abducens, the 
oculomotor, the facial, etc.) and the spinal nerves also may be affected 
(paresthesia, paresis, trophic disturbances, herpes zoster, perforating 



DIABETES 311 

ulcer of the foot, etc.). Epileptiform attacks occasionally occur. Im- 
potence (probably due to spinal degeneration) is common, and may be 
an early symptom. The patient is likely to become nervous, restless, 
irritable, hypochondriacal, or melancholic. 

The most important of the nervous phenomena is coma — which is the 
direct cause of the fatal issue in almost all of the young subjects and in 
from one-half to three-fourths of the older subjects (in unusual cases the 
coma may be not diabetic, but uremic, or due to meningitis, cerebral 
hemorrhage or softening, etc.). Diabetic coma is attributed to acid 
intoxication (/?-oxybutyric acid), of which it is the final stage, and it is 
to be feared in all cases in which ketonuria occurs and when the daily 
output of ammonia (the index of the acidosis) exceeds 3 grams. The 
coma may develop suddenly in the midst of comparatively good health; 
or it may be precipitated by severe exertion, excitement, local infection, 
etc.; or without exciting cause it may come on gradually with weakness, 
headache, restlessness, anxiety, somnolence, nausea, vomiting, syncope, 
KussmauPs dyspnoea, or air-hunger (deep, energetic, long-drawn inspira- 
tion, contrasting strongly with the general asthenia, and short, sighing 
expiration, unassociated with cyanosis, at the beginning at least), 
a sweetish, fruity odor to the breath (excretion of acetone and diacetic 
acid with the breath), and gradually deepening coma. The pulse is 
usually small and rapid, the pupils dilated, the reflexes abolished, and 
the temperature subnormal; convulsions are rare. Death usually ensues 
in from a few hours to a few days; rarely the patient may recover, and 
perhaps succumb to a subsequent attack. 

Complications. — Complications are quite common, being due to the 
hyperglycemia and its attendant impaired nutrition and lessened 
resistance to bacterial infection, acidosis, etc. Diminished resistance 
to bacterial infection (lessened opsonic index) is answerable for the com- 
mon furunculosis, boils, and carbuncles (usually staphylococcic infection), 
tuberculosis, pneumonia, and bronchopneumonia (perhaps followed by 
abscess or gangrene), which are responsible for most of the fatal issues 
not due to coma, but which also may induce the fatal coma. There are 
many sorts of skin eruption, eczema (set up sometimes by intolerable 
itching), urticaria, xanthoma, purpura, etc. Gangrene, especially of 
the leg, is not uncommon in middle-aged or elderly subjects, even in mild 
cases; it is due to atheroma or obliterating endarteritis. 

Generalized arteriosclerosis is common and may be associated witli 
hypertrophy of the heart; rarely, toward the end, in cases of failing heart 
or advanced nephritis, oedema may supervene, but it is uncommon 
on account of the marked polyuria and consequent "dryness" of the 
tissues. Amenorrhoea is common. Conception may occur, but is 
likely to be followed by abortion or aggravation of the disease. Vulvitis, 
vaginitis, urethritis, etc., are common in the female, and balanitis, 
phimosis, etc., in the male. The special senses may become involved— 
amblyopia, amaurosis, retinitis, cataract (especially in young subjects), 
chronic catarrhal deafness (otitis media), etc. 



312 DISORDERS OF METABOLISM 

Diagnosis. — The diagnosis comprises not only the mere recognition of 
the disease and its differentiation from other disorders that resemble it, 
but also the determination of the type and severity of the disorder, of the 
degree of carbohydrate tolerance, of the presence and the degree of 
acidosis, and of the general nutrition of the patient. Polyuria, poly- 
dypsia, polyplagia, emaciation, and such suggestive phenomena as genital 
pruritus, impotence, bilateral sciatica, recurring boils, etc., may suggest 
the disease; but the diagnosis usually, and in the early stages always, 
depends upon an examination of the urine. Too much importance can- 
not be attached to the routine examination of the urine, in all cases of 
diseases, if the early stages of diabetes are to be diagnosticated. 

The carbohydrates include : (1) The monosaccharides or glucoses — 
glucose (dextrose, grape sugar), levulose (fruit sugar), and galactose 
(invert milk sugar); (2) the disaccharides or saccharoses — saccharose 
(cane sugar), maltose (malt sugar), and lactose (milk sugar); (3) the 
polysaccharides or amyloses — starch, glycogen, dextrin, cellulose, and 
certain gums; and (4) the pentoses or five-carbon sugars — arabinose and 
xylose; and glycuronic acid. Of these, only glucose, lactose, maltose, 
levulose, pentose, and glycuronic acid possess clinical importance in the 
present connection. Glucose (dextrose) may be determined by Fehling's 
test, the fermentation test, the phenylhydrazin test, and dextrorotation 
of polarized light (in the polariscope) ; but one must also exclude certain 
non-carbohydrate reducing substances, such as uric acid, creatinin, 
alkapton, and certain drugs (for details one should refer to books on 
clinical laboratory diagnosis). 

Having determined the presence of glucose in the urine, it is advisable 
to ascertain whether the condition is: (1) Toxic glycosuria, such as may 
follow the administration of anesthetics, or certain drugs and poisons, 
such as phloridzin, chloral, morphine, coal-tar products, etc., or develop 
in the course of or following pregnancy, some infection, etc. ; (2) neurotic 
glycosuria, such as may be due to divers emotional or other disturbances, 
shocks, etc.; or occur in association with different nervous diseases; 
(3) alimentary glycosuria (the inability to metabolize 100 grams of 
glucose taken at one time without the appearance of glucose in the 
urine); or (4) true diabetic glycosuria. The toxic, neurotic, and ali- 
mentary cases are transitory and intermittent; as a rule, the amount 
of sugar excreted is small, and the condition may entirely disappear: 
but many of the cases bear a more or less intimate relationship to true 
diabetes, of which they may be an early stage or ill-developed form, and 
to which they may progress. 

From a diagnostic, prognostic, and therapeutic standpoint it is im- 
portant in the case of true diabetes (continuous glycosuria associated 
with the other mentioned symptoms) to determine the type, whether 
mild, intermediate, or severe; that is, to determine the carbohydrate 
tolerance. Mild cases are those in which some degree of carbohydrate 
tolerance is maintained; that is, 100 grams of glucose can be metab- 
olized without the development of glycosuria, and no disturbance 



DIABETES 313 

in fat metabolism is present; that is, there is no ketonuria. Inter- 
mediate cases are those in which the carbohydrate tolerance is almost 
if not quite lost (less than 30 to 50 grams) ; that is, the urine becomes 
aglycosuric on a carbohydrate-free diet continued for a week or more; 
and there is also some disturbance of fat metabolism, shown in aceto- 
nuria and diaceturia from time to time, but especially when the 
patient is on a carbohydrate-free diet. Severe cases are those in which 
the carbohydrate tolerance is entirely lost; that is, the urine does 
not become aglycosuric, even when a carbohydrate-free diet has been 
continued for several weeks, although aglycosuria may be produced 
by restriction of the protein intake; and ketonuria (including often 
/?-oxybutyric acid) is a constant feature. The severity of the case is to 
be determined not so much by the output of glucose, assuredly not 
by the percentage output, as by the output compared with the carbo- 
hydrate intake. In some cases of total carbohydrate intolerance sugar 
may be found in the urine on a fat-protein diet in the proportion of 
3.65 to 1 of nitrogen (the fatal ratio, Mandel and Lusk). The majority 
of cases of diabetes are mild, but they are most common in elderly and 
obese subjects; intermediate cases are common in middle life; severe 
cases are most common in youthful and in thin subjects. 

The acidosis may be determined by Gerhardt's, Arnold's, or Hart's tests 
(for diacetic acid and acetone), by the Huppert-Messinger quantitative 
test, by levorotation of polarized light after complete fermentation of the 
urine, by determining the ammonia output, and roughly by the amount of 
sodium bicarbonate required to render the urine alkaline (normally 5 to 
10 grams, Blum). The general condition of the patient is to be determined 
by repeated physical examination and determination of the body weight. 
Diabetic coma may be distinguished from uremic coma by ketonuria, per- 
haps glycosuria, fruity odor to the breath, and the characteristic Kuss- 
maul dyspnoea; albuminuria and the cardiovascular and other signs of 
chronic nephritis are often present, and may at first be confusing. 

Prognosis. — The course of the disease is rarely acute (several weeks); 
usually it is chronic — several years to many years (twenty or more). 
The prognosis varies with the severity of the case: it is bad in youthful 
subjects (in infancy, childhood, and adolescence); in thin rather than 
obese subjects; in the event of marked and rapid loss of flesh (despite 
the ingestion of a large amount of food); in the event of carbohydrate 
intolerance, marked glycosuria, ketonuria, non-response to treatment, 
and infectious complications. Coma is almost invariably fatal. The 
prognosis is favorable in elderly obese subjects; in cases with fair or 
moderate carbohydrate tolerance, slight glycosuria, and no ketonuria; 
in the absence of complications; and in the event of response to treat- 
ment (lessening of glycosuria and increase in weight). 

Treatment. — The treatment is almost, if not quite, wholly dietetic. 
General hygienic measures; a life of comparative ease and quiet, free from 
undue professional or business exactions, worry, and emotional and other 
disturbances; a moderate amount of regulated exercise (which in some, 



314 DISORDERS OF METABOLISM 

especially mild, cases appears to increase sugar metabolism, but which 
may have a contrary effect in severe cases); now and then a course of 
treatment at some one of the well-known spas; and drugs — each has its 
place in treatment, but the physician must individualize; he must treat 
the patient, not the disease. 

Diet. — Since the patient has more or less lost the ability to metabo- 
lize carbohydrates, and we are unable directly to influence the carbohy- 
drate metabolism, it becomes necessary to nourish him largely on a 
fat-protein diet. The difficulty in doing this is apparent from the fact 
that a healthy subject ordinarily derives almost one-half of his heat and 
energy from carbohydrates; that this is largely or wholly lost to the dia- 
betic through the glycosuria; that it is difficult to supply this deficiency 
with a fat-protein diet (which is not the most palatable); and that 
continuation of the hyperglycemia results in a decreased tolerance of the 
tissues for carbohydrates — as, on the contrary, lessening of the hyper- 
glycemia results in an increased tolerance; and that a carbohydrate-free 
diet is likely to lead to a dangerous acid intoxication. The permissible 
and the prohibited foods are mentioned in Table I, which as well as 
the other tables appended have been arranged by T. C. Janeway. 

In the treatment of every diabetic subject the first essential is to deter- 



Table I. — General Diabetic Diet List. 

May take freely: Soups — all meat soups and broths; may add vegetables allowed, egg, or 
cheese. Meats — all fresh, smoked, or cured meats (except liver), poultry, and game, without 
sauces or gravies containing flour; pate de foie gras. Fish — all kinds of fish, except oysters, 
clams, and scallops, cooked without bread crumbs or meal; dried, salted, smoked, or pickled 
fish. Eggs — prepared in any way without flour. Fats — butter, lard, suet, olive oil, or other 
fats. Cheeses — all kinds, especially cream, Swiss, English, and pineapple cheese. Vegetables 
and salads— asparagus, beet greens, Brussels sprouts, cabbage, cauliflower, celery, chicory, 
cresses, cucumbers, egg-plant, endive, kohl-rabi, leeks, lettuce, okra, pumpkin, radishes, 
rhubarb, salsify, sauerkrout, spinach, string beans, tomatoes, vegetable marrow. Pickles made 
from the above-mentioned vegetables, unsweetened; ripe olives. Fungi — mushrooms and 
truffles. Cream — not over three ounces a day. Condiments — salt, pepper, cayenne, paprika, 
curry, cinnamon, cloves, English mustard, nutmeg, caraway, capers, vinegar, and the piquant 
sauces in small quantities, unless specially forbidden. Desserts — jellies made from gelatine; 
custards and ice cream made with eggs and cream; all sweetened with saccharin and flavored 
with vanilla, coffee, or brandy. The following recipes for desserts are suggested: Baked cus- 
tard— 1 egg, 1H ounces of cream, 2)4, ounces of water; two or three J^-grain saccharine tablets, 
8 drops of vanilla essence; beat up well, pour into a buttered dish, grate a little nutmeg on 
top, and bake twenty minutes. Coffee ice cream — \]4, ounces of cream, 1}4 ounces of water, 
1 ounce of strong coffee, two or three J^-grain saccharine tablets; dissolve; add 1 egg, well 
beaten; mix in a saucepan and beat slowly with stirring until it thickens; set aside until cool; 
then freeze. Nuts — butternuts. Beverages — tea or coffee, sweetened with saccharin, and 
with the portion of cream allowed; whiskey, brandy, rum, and other distilled liquors up to 3 
ounces a day; light Rhine or Moselle wine, claret, or Burgundy up to 16 ounces a day; mineral 
waters of all kinds; lemonade in small quantity, sweetened with saccharin. 

Articles prohibited, except as prescribed in the accessory diet (carbohydrate equivalents, Table IV) : 
Sugars and sweets of every kind; pastry, puddings, preserves, cake, and ice cream; bread and 
biscuit of all kinds, toast, crackers, and griddle cakes; cereals, such as rice, oatmeal, sago, 
hominy, tapioca, and barley; macaroni, potatoes, carrots, parsnips, beans, peas, beets, green 
corn, and turnips; fruit of all kinds, fresh and dried; soups, sauces, or gravies thickened 
with flour or meal, or made with milk; beer, ale, porter, all sweet wines, sherry, or port 
wine, sparkling wines, cider, and liqueurs; milk, chocolate, or cocoa; all sweet drinks and 
soda water, 






DIABETES 315 

mine the carbohydrate tolerance and the degree of acidosis (if there be 
any) ; the carbohydrate tolerance should be redetermined at least every 
two months in mild and intermediate cases, and perhaps more fre- 
quently in the severe cases. To determine the carbohydrate toler- 
ance, the patient should be put upon a fixed fat-protein diet of suffi- 
cient caloric value to maintain strength and body weight; that is, 35 
large calories per kilogram of body weight (a man weighing 70 kilo- 
grams — 150 pounds — requires about 2500 calories per day). The carbo- 
hydrates should be withdrawn gradually (three to seven days, depending 
upon the severity of the case), since sudden withdrawal may result in a 
severe, perhaps fatal, acidosis. While determining the carbohydrate 
tolerance, the presence and the degree of acidosis should be inquired 
into, and if present the patient should be given one-half to one ounce of 
sodium bicarbonate daily. A suitable fat-protein diet is indicated in 
Table II. To this fat-protein diet 100 grams (3 ounces) of white bread 
(55 per cent, of carbohydrate) in three equal portions should be added. 
The bread should be gradually withdrawn until the urine has become 
sugar-free; if the patient is not aglycosuric when the bread has been 
entirely withdrawn, the diet without bread should be continued for one 
week or more, in the hope that the urine will become sugar-free. If the 



Table II. — Standard Strict Diet. 

Breakfast: Coffee with \Y ounces cream; 2 eggs cooked with Y ounce butter; 3 ounces ham. 
Luncheon: Bouillon with 1 raw egg; 3 ounces sirloin steak, chicken, or leg of lamb; 1 ounce 
bacon; vegetable from list, 2 tablespoonfuls, with Y ounce butter; dessert made with 1 egg and 
\Y ounces cream; 6 ounces wine, or 1 ounce whiskey or brandy. 
Afternoon tea with Yi ounce cream. 

Dinner: Any clear soup; 3 ounces fish (salmon, shad, or mackerel), with Yl ounce butter; 
Y pound roast pork, beef, mutton, turkey, or lamb chops; vegetables from list, 2 tablespoon- 
fuls, with Yz ounce butter; salad with Yi ounce oil in dressing; 1 ounce cheese, English, pine- 
apple, Swiss, or full cream; 6 ounces wine, or 1 ounce whiskey or brandy; demitasse of coffee. 

Protein = 126 grams; 515 calories 

Fat = 222 grams; 2065 aalories 

Carbohydrate =15 grams; 60 calories 

Alcohol =30 grams; 210 calories 

2850 

Table III. — Standard Diet with Restricted Protein. 

Breakfast: Coffee with \Y ounces cream; 2 eggs with Yl ounce butter; 1 ounce bacon. 
Luncheon: 2 eggs; 1 ounce bacon; 2 ounces lamb chops (1), ham (2), beefsteak (3), chicken 
(4), or fish (5) broiled with Yi ounce butter (each day select meat with same number for 
luncheon and dinner) ; vegetable from list, 2 tablespoonfuls, with H ounce butter; dessert made 
with 1 egg and 1Y ounces cream; 6 ounces wine or 1 ounce whiskey or brandy. 
Afternoon tea with Y ounce cream. 

Dinner: Any clear soup; Y pound roast pork (5), beef (4), mutton (3), turkey (2), chicken 
(1), or lamb (1); (each day select meat with same number for luncheon and dinner); vegetables 
from list, 2 tablespoonfuls, with Y ounce butter; salad with Y ounce oil in dressing; 1 ounce 
cream cheese; 6 ounces wine or 1 ounce whiskey or brandy; demitasse of coffee. 

Protein =82 grams; 334 calorics 

Fat = 215 grams; 2008 calorics 

Carbohydrate =15 grams; 60 calories 

Alcohol =30 grams; 210 calories 

2612 



316 DISORDERS OF METABOLISM 

urine becomes sugar-free, gradually increasing, weighed amounts of white 
bread may be added to the diet until sugar is again excreted. Should 
the patient continue to excrete sugar on the fat-protein diet (without 
bread), the protein intake must be reduced, since considerable protein 
intake increases the glycosuria. A suitable diet with restricted protein 
is that of Table III. 

The foregoing procedures will determine the carbohydrate tolerance 
(expressed in weighed amounts of white bread), as well as the presence 
or absence of acidosis, and permit of a classification of the case — mild, 
intermediate, or severe. As regards the acidosis, subjects who tolerate 
100 grams or more of bread rarely have acidosis; those who tolerate 
less carbohydrate may or may not exhibit ketonuria, but the ketonuria 
that develops during this experimental withdrawal of carbohydrates 
lasts only a few days, as a rule; the diacetic acid disappears, and the 
amount of acetone is not in excess of the normal. 

The subsequent treatment of- the patient varies with the type of the 
disease, but the main indications are to maintain nutrition and body 



Table IV. — Table of Carbohydrate Equivalents. 

Amount in ounces 

Per cent, equal to 1 ounce 

Article. carbohydrates. white bread. 

Breads: White 51-55 1 

All other 47-53 1 

Rolls and biscuit 52-60 1 

Cornbread 46 \y% 

Crackers, average 69-72 % 

Cereals: Oatmeal, boiled 11.3 5 

Hominy, boiled 17.8 3 

Macaroni, boiled 15.8 3J4 

Rice, boiled 24.4 2V 8 

Tubers and Legumes: Potatoes, cooked .... 18-20 3 

Parsnips 13 4 

Beans, baked 20 2% 

Beans, lima, cooked 20 2% 

Peas, green, cooked 15 3J^ 

Milk 4-5 10 

Fruits: Apples, apricots, and pears 12-14 4 

Cherries 15 3J^ 

Huckleberries 16 3J4 

Plums 20 2H 

Bananas 22 2Y 2 

Nuts: Filberts 12 4H 

Almonds 15 3}4 

Peanuts 22 2*A 

Table V. — Green Days. 

Breakfast: 1 egg, boiled or poached; cup of black coffee. 

Dinner: Spinach with a hard-boiled egg; }4 ounce bacon; salad, with Yi ounce oil; 6 ounces 
of wine or 1 ounce of whiskey or brandy. 

4.30 p.m.: Cup of beef tea or chicken broth. 

Supper: 1 egg, scrambled, with tomato and a little butter; Y. ounce bacon; cabbage, sauer- 
kraut, string-beans, or asparagus; cup of tea; or white wine, 4 ounces; or whiskey or brandy, 
1 ounce. 

Y>, ounce of sodium bicarbonate in the twenty-four hours. 

Carbohydrates = about 5 grams. Calories = 575. 



DIABETES 317 

weight, to lessen the hyperglycemia (of which the glycosuria affords a 
clinical measure), and to prevent or control the acidosis. Mild cases, 
in which the carbohydrate tolerance is 100 grams or more of white 
bread, should be kept within their limit. Physicians who prefer gluten 
bread should not prescribe it under the misapprehension that it is harm- 
less; most of those on the market contain from 30 to 70 per cent, of 
carbohydrate; ordinarily it is better to give a weighed amount of white 
bread of known carbohydrate content. The patient may be permitted 
to vary the carbohydrates of his diet in accordance with his desires and 
his metabolic activities — which in individual cases is not alike for all 
carbohydrates. Table IV shows some permissible carbohydrates and 
their equivalents in terms of white bread. In the intermediate cases, 
the diet in general should conform to that of Table II, with the addition 
of such small amount of carbohydrate as may be found to be within the 
patient's capabilities to metabolize. Considerable bacon, fat meats (fat 
beef, pork, mutton, etc.), and fish (salmon, etc.), up to a total of not 
more than 150 grams (5 ounces) daily, butter, thick cream, cheese, oil, 
etc., are especially to be used. The digestion of the considerable amount 
of fat and the prevention of diarrhoea from imperfect digestion of fat may 
be facilitated by a moderate amount of alcohol, as suggested in Tables I, 
II, and III. In severer cases the difficulties are increased; the protein 
must be reduced, and one may not add carbohydrates. Study and re- 
arrangement of the diet, however, will permit one to nourish the patient 
sufficiently on a very low protein diet (100 grams or less). Idiosyncrasies, 
however, must be met — some patients cannot, others will not, adhere to the 
prescribed diet, others fail in nutrition, or acidosis develops, in which 
cases, heterodoxical as it may seem, it is better that the patient have a 
little sugar in his urine than that he fail in flesh and strength or run 
the risks of acid intoxication. Now and then a diet containing very little 
protein is serviceable: largely broths (the hunger days of Naunyn), or 
green vegetables, eggs, bacon, butter, black coffee, and alcohol (the green 
days of von Noorden, Table V). 

Good results have been reported from time to time by a milk cure, 
Mosse's potato cure, and von Noorden's oatmeal cure. The last- 
mentioned consists of 250 grams of oatmeal, salted to suit the taste, and 
three to four quarts of water, cooked for two hours on a moderate fire; 
thereupon 250 to 300 grams of butter and 100 grams of a vegetable 
albumin, such as roborat, gliden, rice albumin, etc., is added (six to 
eight eggs may be substituted for the albumin in the country). This is 
to be taken in divided portions during the twenty-four hours, with a little 
black coffee or alcohol. Von Noorden recommends the treatment in 
cases of moderate severity, four or five times a year, for a week — thus : 
one vegetable day, three oatmeal days, two vegetable days. The return 
to the usual diabetic diet must be gradual, since otherwise increased 
glycosuria and coma may ensue. 

Drugs. — The drug treatment of diabetes is notoriously inefficient, 
although drugs have their place in the treatment; but without proper 



318 DISORDERS OF METABOLISM 

dietetic regulation drugs are worse than useless. Opium, codeine, 
and arsenic often seem to be of much service; they appear to favor 
oxidation, lessen glycosuria (perhaps by preventing protein destruction), 
and increase the general well-being of the patient. The bromides are 
of service in many of the nervous manifestations. Tonics, such as 
iron, quinine, strychnine, etc., are often useful. Jambul, chimophila, the 
salicylates, etc., have been extolled from time to time. The alkalies 
are of distinct service — the alkaline mineral waters and the carbonate, 
bicarbonate, citrate, tartrate of sodium. In the event of acetonuria one- 
half to one ounce of sodium bicarbonate should be given daily, and 
twice or thrice as much in impending coma. Developed coma is usually 
fatal, but it is sometimes relieved by intravenous injections of 2 to 4 per 
cent, of sodium carbonate in physiological saline solution. The compli- 
cations are to be treated on general principles. 

DIABETES INSIPIDUS. 

(Polyuria.) 

Diabetes insipidus is a chronic disorder characterized by the passage 
of large amounts of non-saccharine and non-albuminous urine of low 
specific gravity. 

Etiology. — The disorder is most common in males between the 
twentieth and the thirtieth year; more than half of the cases occur be- 
tween the tenth and the fortieth year. Some cases seem to be hereditary, 
or several cases occur in the same family. Two types of polyuria may 
be differentiated — the secondary or symptomatic and the primary or 
idiopathic. Symptomatic polyuria is especially common: (1) In diabetes, 
chronic interstitial nephritis, after drinking large amounts of water, etc., 
in organic and functional disorders of the cerebrospinal and sympathetic 
nervous system, such as trauma, syphilis (gumma, basilar meningitis), 
tumors (especially of the floor of the fourth ventricle), hemorrhage, 
hydrocephalus, lesions of the medulla, of the trapezoid body of the pons, 
or of the middle cerebellar lobe, etc., fright, emotional disturbances, 
hysteria, neurasthenia, psychoses, epilepsy, alcoholism, etc.; (2) during 
or after infections (typhoid, typhus, malarial or scarlet fever, tuberculosis, 
diphtheria, measles, etc.); and (3) in conditions of general ill health 
from overwork, mental anxiety, poor nutrition, etc. The idiopathic 
cases are those that develop without obvious or discoverable cause. 

The nature of the disease is not well understood. The basis of it is 
believed to be a functional incapacity of the kidneys (unassociated with 
noteworthy structural alterations), due to disturbance of the nervous 
or vascular mechanism (vasodilatation unaccompanied by rise of the 
general arterial pressure), in consequence of which the kidneys are 
unable to excrete urine containing a normal percentage of solids; the 
normal amount of solids can be excreted only in association with the 
passage of a large amount of urine, in the absence of which concentration 
of the blood occurs. Increase in the protein intake does not cause, as it 



DIABETES INSIPIDUS 319 

does in health, an increase in the specific gravity of the Urine, but an 
increase in the amount of urine, the proportion of urea remaining con- 
stant. Similar results follow variations in the sodium chloride intake. 
Occasionally diabetes insipidus is said to develop into diabetes mellitus, 
and vice versa, but usually this is a misinterpretation of surface 
phenomena. 

Pathology. — There are no constant or characteristic lesions. Divers 
lesions of the brain are found in about one-third of the cases. The kid- 
neys may be enlarged and congested, and the renal pelves, ureters, and 
bloodvessels dilated and hypertrophied. 

Symptoms. — As a rule, the onset of the disease is insidious; in some 
cases, as after a fright, etc., there may be a sudden, usually transitory 
polyuria; in other cases, as after trauma, the onset may be abrupt, but 
the course protracted. The characteristic phenomenon is the passage of 
a large amount (5, 10, 20, or more liters daily) of urine, which is pale in 
color and of low specific gravity (1005 to 1001 or less); the total solids are 
about normal; albumin and sugar are absent, except in rare circum- 
stances, and then are present only in traces and temporarily. Thirst is 
an almost constant symptom and may be the first noteworthy manifes- 
tation; it is the result and not the cause of the polyuria. The appetite 
may be poor, normal, or excessive; the stomach may become dilated; 
the mouth and the skin usually are dry; constipation is common. Head- 
ache, nervousness, irritability, loss of sexual power, and other nervous 
manifestations may occur, the general health may remain for a long 
time unaffected (depending upon the actuating cause); but emaciation 
and loss of strength sometimes supervene. 

Diagnosis. — The diagnosis is easy. Symptomatic cases should be 
readily recognized by attention to the causative factors ; the frequency of 
syphilis as an etiological factor should be borne in mind. Diabetes 
mellitus may be excluded by the absence of hyperglycemia, glycosuria 
(and high specific gravity), carbohydrate intolerance, ketonuria, and the 
common complications. Chronic interstitial nephritis may be excluded 
by the absence of albuminuria, casts, and the cardiovascular, retinal, and 
uremic manifestations of nephritis ; in addition, the specific gravity of the 
urine is usually higher and the amount less than in diabetes insipidus. 

Prognosis. — The duration and prognosis vary with the cause and type 
of the disease. Recovery, except in the obviously transitory cases, is 
unlikely, but the patient may live for many years. Death often ensues 
from complicating infections. 

Treatment. — As low a protein and sodium chloride intake as is con- 
sistent with the maintenance of strength and weight should be given. 
It is not necessary or advisable to restrict the fluid intake, since it results 
in retention of the urinary solids and other harmful consequences. The 
iodides are often of marked benefit even in apparently non-syphilitic 
cases. Strychnine and vasoconstrictors, such as ergot, belladonna, etc., 
are often followed by benefit; adrenalin hypodermicly or intravenously 
may be tried. Opium and valerian also are of value in some cases. 



320 DISORDERS OF METABOLISM 

GOUT. 

(Podagra.) 

Gout is a chronic disorder of metabolism attended by marked excess 
of uric acid in the blood, and the deposition in and about the joints, as 
well as in other cartilaginous and fibrous tissues of the body, of crystalline 
sodium biurate. 

Etiology. — While the exact disturbances of metabolism occurring in 
gout are still the subject of much study and discussion, certain predis- 
posing factors are commonly recognized. Of these, heredity is probably 
the most important. Although it is generally conceded that gout may be 
acquired, that is, that it occurs in the absence of gouty ancestry, and 
although not all descendants (children and grandchildren) of gouty 
subjects become gouty, the common opinion is that at least 50 to 60 per 
cent, of gouty patients suffer for the sins of their ancestors. Futcher, 
however, who states that gout is much more common in this country than 
is generally believed, being often unrecognized, believes that it is much 
more frequently acquired than inherited, since not more than 31 per cent, 
of his patients had gouty ancestors. Gout is much more common in 
males than in females, and transmission is through the male rather 
than the female members of the family. In the female the disease is 
almost always inherited. It is more common in the white than in the 
colored race. It usually makes its appearance during the fourth decade, 
and then continues more or less through the remainder of life; it may 
however, develop later, and rarely earlier, sometimes during the second, 
and even the first decade. Continued overindulgence in alcoholic bever- 
ages is an important etiological factor, fermented liquors, such as beer, 
ale, and porter, and wines, such as sherry, port, and champagne, being 
much more injurious than distilled liquors, such as whiskey, brandy, gin, 
rum, etc. Something more than the mere percentage of alcohol seems to 
be of significance. Overeating combined with insufficient exercise 
strongly conduce to gout; and it is more the mere overeating as such, 
rather than the special kind of food (such as red meats, for instance, 
long but perhaps erroneously too much blamed), that does the harm. 
Gout is by no means confined to the wealthy and idle class, since "in 
England the combination of poor food, defective hygiene, and an exces- 
sive consumption of malt liquors makes 'the poor man's gout' a common 
affection" (Osier). Chronic lead poisoning is also an important etiolog- 
ical factor, though less so in this country than in England; how it acts, 
whether by causing arteriosclerosis, by lessening the alkalinity of the 
blood (most saturnine patients seem to have an excess of uric acid in their 
blood), or by provoking trophic changes through the medium of the 
nervous system, is not definitely known. 

Despite considerable patient inquiry and investigation, the ultimate 
factor in the disorder of metabolism provoking the gouty manifestations 
has not yet been definitely determined. It is generally conceded that 



GOUT 321 

gout results from faulty metabolism (largely defective oxidation) of the 
nitrogenous foodstuffs and of the nitrogenous products of tissue waste, 
and that, in some way or other disturbances in the formation or elimi- 
nation (or both) of uric acid is, directly or indirectly, in large part at 
least, the proximal causative factor. Uric acid (C 5 H 4 N 4 O s ), as well as 
other nitrogenous compounds, xanthin, hypoxanthin, adenin, and guanin, 
are derived from the nuclei of the leukocytes and other cells of the bodv 
(endogenous purin bodies) and from the nuclei of ingested food (exo- 
genous purin bodies). Closely related to these are other substances 
(containing carbon, hydrogen, nitrogen, and oxygen (?)), known as 
heteroxanthin, paraxanthin, episarkin, carnin, and epiguanin. Collec- 
tively, that is, including uric acid, they are known as the xanthin bodies, 
the nuclein bodies (because of their derivation), the alloxuric bodies 
(because they contain an alloxan and a urea nucleus), and the purin 
bodies (because they are derived from or may be prepared synthetically 
from purin, C 5 H 4 N 4 ); excluding uric acid, they are known as the xanthin, 
nuclein, alloxuric, or purin bases. Their derivation may be thus repre- 
sented graphically : 

Nuclein 
I 



I I 

Albumin Nucleic acid 

I 



! I 

Phosphoric acid Mother substance 

I 



I I 

Uric acid Xanthin, nuclein, alloxuric, or purin bases 

How uric acid circulates in the blood under normal conditions is not 
definitely known. It is said to form three groups of salts, which, with 
sodium as the base, are as follows : (1) Neutral sodium urate, merely a 
laboratory compound; (2) acid sodium urate, or sodium biurate, which 
does not occur physiologically, though this is the form in which the 
uric acid is deposited in the gouty tophi; and (3) sodium quadriurate, 
which is loosely combined, readily soluble, and the form in which Sir 
William Roberts and many others believe the uric acid circulates in the 
blood. Minkowski believes that the uric acid circulates in combination 
with the purin base, nucleotin-phosphoric acid. In health an adult of 
average weight on a mixed diet excretes from 0.4 to 1 gram of uric 
acid, approximating 0.7 gram on an average; and the ratio of uric acid 
to urea, though it varies much, averages from 1 to 50 to 1 to 70. 

In gout, according to Minkowski: (1) The daily excretion of uric acid 
in the intervals between the acute attacks ranges within the same limits 
as does the excretion in healthy individuals; (2) in chronic gout, even 
in those cases in which there is marked deposition of biurates in the 
tissues, a constant variation from the normal amount of uric acid 
excretion in any one direction has not been definitely proved; and (3) 
immediately preceding an acute attack there is regularly a diminution in 
21 



322 DISORDERS OF METABOLISM 

the amount of uric acid eliminated in the urine, whereas during and after 
the attack the uric acid output is increased. Futcher disagrees with 
these statements in having found almost always a marked diminution in 
the uric acid excretion in the intervals between acute attacks in chronic 
tophaceous gout. The blood in gout contains a marked excess of uric 
acid, and although there has been and still is much discussion as to 
whether this is due to increased formation, diminished destruction or 
oxidation, or diminished excretion by the kidneys, the weight of opinion 
recently tends to support the view that it is due to deficient excretion by 
the kidneys, and this in turn has been attributed to " functional" dis- 
turbances independent of apparent organic disease, to the nephritic 
lesions so common in gout, and by Minkowski and His to the circum- 
stance (not proved) that the uric acid in gout may circulate in combina- 
tion different from that of health and more difficult of elimination by the 
kidneys. 

Heretofore too little attention has been paid to the excretion of the 
purin bases in gout. Since it has been shown that normally about nine- 
tenths of the purin bodies eliminated is uric acid, and about one-tenth 
the purin bases, and since there is no evidence that this relationship is 
disturbed in gout, it is not unlikely, as maintained by Kolish, that at 
least certain of the gouty phenomena may be due to these purin bases. 
As regards the phosphoric acid elimination, Futcher has shown that in 
the intervals between the attacks in chronic gout it falls far below the 
lower limits for the normal, and that with the onset of the acute attack, 
concurrently with the increase in the uric acid elimination, there is a 
parallel rise of the phosphoric acid elimination to the average or even to 
the upper limits for the normal. Others, however, have obtained some- 
what divergent results. 

Pathology.— In addition to a marked increase of the uric acid in the 
blood, a constant feature of the disease first pointed out by Garrod, the 
joints present the most characteristic lesions of the disease — the deposi- 
tion of crystalline sodium biurate in the cartilages, synovial membranes, 
tendons, ligaments, and bursa?. The metatarsal-phalangeal joint of the 
great toe is most frequently involved, and the lesions may remain confined 
to this joint for a long time; later, however, the metatarsal, the ankle, the 
small joints of the hands and fingers, and the knee and the wrist may 
become involved, but sometimes the lesions affect only the lower extremi- 
ties. Similar deposits occur also in the helix of the ear, as well as in the 
cartilages of the nose, eyelids, and larynx ; they have been observed in the 
periosteum (over the sacrum and elsewhere), and in the tendons (the 
tendons of the hand and forearm, Achilles tendon, plantar surface of the 
foot, etc.). The deposits of sodium biurate occur in, rather than on, 
the surface of cartilage, being always covered by a thin layer of carti- 
lage, through which they present as white, "chalky" deposits, or tophi. 
Whether there is a primary tissue necrosis with a secondary deposition of 
the sodium biurate, as maintained by Ebstein, or vice versa, as maintained 
by His and Mordhorst, has not been definitely determined. Ebstein 



GOUT 323 

maintains that the tissue necroses are always primary, that he has found 
them without any uratic deposits, and that they are acid in reaction — 
whence the ready deposition of the soluble and loosely combined quadri- 
urate as the insoluble crystalline biurate. Sir William Roberts believes 
that the deposits occur especially in the cartilages, because in them the 
nutritional currents are slowest and least abundant, the temperature 
lowest, and in the articulating surfaces the percentage of sodium chloride 
highest. As the disease advances the periarticular tissues (ligaments 
and fibrous tissues) become invaded, and often large tophi or " chalk 
stones" are formed, which, together with the fibrous thickenings, lead to 
fixation and much distortion of the joints. Though usually covered by 
skin, the tophi may cause ulceration of overlying structures, and small, 
nodular, "chalky" masses may be discharged externally. True bony 
outgrowths are found about the margins of certain joints in far advanced 
cases. 

The kidneys show the changes of chronic interstitial nephritis (the 
gouty kidney) or sometimes the type described as the arteriosclerotic 
kidney. Whitish streaks, evidences of deposits of sodium biurate, may be 
found in the papillae, and in and between the uriniferous tubules. Gen- 
eral arteriosclerosis is common ; indeed, gout is one of the most frequent 
causes of arteriosclerosis. Hypertrophy of the left ventricle is a usual 
concomitant. Not infrequently myocardial degeneration leading to 
dilatation of the heart follows, and is quite often associated with unusual 
atheroma of the arch of the aorta and the orifices of the coronary arteries. 
Deposits of sodium biurate have been found in the heart valves. Gouty 
pericarditis sometimes occurs toward the close of life, and may be the 
direct cause of death. Emphysema of the lungs is common, and chronic 
bronchitis and asthma may supervene. Crystals of sodium biurate may 
be found in the sputum. Neusser's perinuclear basophilic granules are 
now known to be artefacts. Despite the chronic course of the disease, no 
noteworthy anemia, as a rule, develops. 

Symptoms. — Three varieties of gout are usually distinguished, acute 
gout, chronic gout, and irregular gout. 

Acute Gout. — Acute gout may be abrupt on onset, but, as a rule, it 
is preceded for several days, or at least a few hours, by vague pains in the 
joints or muscles, irritability of temper, mental depression, insomnia, 
dyspepsia, and scantiness of urine (containing a deficiency of uric acid). 
Occasionally, however, such prodromal manifestations are absent. The 
attack usually begins abruptly in the early morning hours, the patient 
being awakened by a sharp excruciating pain in the ball of the great toe. 
The joint swells rapidly, and becomes red, hot, extremely tender, and the 
surrounding skin cedematous and shiny. Fever, 102° to 103° F., usually, 
but not always, accompanies the attack. As the morning wears on the 
symptoms abate, and the patient may become tolerably comfortable; 
but the morning of the succeeding day, usually of each succeeding day 
for a week or thereabouts, witnesses a recurrence of the severe symptoms, 
which, however, progressively diminish in intensity. Just prior to and 



324 DISORDERS OF METABOLISM 

during the early part of the attack the uric acid output is diminished, 
but later and for a short time after the attack it becomes increased. In 
addition, the urine is scanty, acid in reaction, of increased specific gravity, 
and heightened color, and it may contain a trace of albumin or of 
sugar (transitory). Following the subsidence of the acute manifestations, 
the patient soon regains his former health — indeed, he may feel much 
improved. The affected joint soon returns to its normal condition, 
except in cases of chronic gout, in which deformity sooner or later ensues. 
The acute attack does not always involve the great toes; occasionally 
other joints, such as the wrist, knee, or the small joints of the fingers may 
suffer; and the lesions are not always confined to a single joint, both 
great toes, for instance, being occasionally affected. The attacks recur 
at varying intervals — weeks, months, or even years — but with the lapse of 
time the intervals, as a rule, become progressively less, and the patient 
gradually develops chronic gout. 

Occasionally the local manifestations of gout disappear or improve 
rapidly, and concurrently herewith serious symptoms referable to the 
internal organs develop — a condition to which the term retrocedent or 
suppressed gout is applied. The symptoms may be gastro-intestinal — 
abdominal pain, vomiting, diarrhea, with weakness, faintness, and a 
rapid, feeble pulse, progressing occasionally to death; or they may be 
cardiac — precordial pain, dyspnea, and palpitation (doubtless in some 
cases true angina pectoris) ; or they may be cerebral — mental excitement 
or depression, apoplexy, delirium, or coma — in many cases probably 
uremic. 

Chronic Gout. — In consequence of repeated attacks of acute gout, 
commonly with gradually decreasing intervals, the symptoms, though 
less acute, become more continuous. Urates become deposited in the 
articular cartilages, later in and about the ligaments and periarticular 
fibrous tissues; these tophi, which often become extreme, together with 
fibrous thickenings, occasion fixation and marked swelling and deformity 
of the joints. Usually the feet are first involved; later the hands, fingers, 
wrists, knees, etc., may show most extensive changes. As already 
observed, the tophi may ulcerate through the skin, and chalky deposits 
may be exposed or even discharged externally. Similar deposits are 
found in the cartilages of the ear, and elsewhere in the tendinous and 
fibrous tissues throughout the body. The patient is usually dyspeptic. 
Gradually arteriosclerosis develops, and the patient presents the com- 
mon cardiac and vascular manifestations of this condition. Soon also 
the evidences of chronic interstitial nephritis present themselves: the 
urine increases in amount, is of low specific gravity, and contains a slight 
amount of albumin and a few hyaline casts. Aside from the incapacities 
attendant upon the joint deformities, the patients often exhibit unusual 
physical and bodily vigor for a long time. The chronic course of the dis- 
ease is sometimes interrupted by acute exacerbations of unusual severity. 
The final end is not infrequently determined by inflammations of any of 
the serous membranes, or by uremia. 



GOUT 325 

Irregular Gout. — Irregular gout is a term applied to an ill-assorted 
group of symptoms that are found in persons who once have had gout, 
or who, though they may never have suffered from gout, yet are pre- 
disposed by heredity or other factors to its development: a condition to 
which the term gouty diathesis or lithemia is often applied, but which 
more than anything else represents a hodge-podge of diagnostic errors. 
Thus, there may be manifestations of catarrh of the gastro-intestinal 
tract, and the gouty stomach, the torpid liver, and biliousness are favorite 
ailments of certain physicians skilled in their treatment. In other cases 
the urine is lessened in amount, high colored, and uric acid crystallizes 
out on standing — a circumstance to which undue importance has been 
attributed. Other disorders ascribed to the same condition comprise 
eczema, headaches, paresthesias, itching of the palms of the hands and 
the soles of the feet, cramps in the legs, itching eyeballs, conjunctivitis, 
iritis, retinitis, tonsillitis, etc. 

Diagnosis. — Typical acute gout can scarcely be mistaken for anything 
else. In atypical cases, as, for instance, when the feet are not involved, 
or when there is polyarthritis, the differentiation from rheumatic fever 
may be determined by a tophus in the ear, but the mode of life, the 
occupation, hereditary factors, the absence of fever, and the condition 
of the urine may be of contributing diagnostic importance. Systematic 
search for tophi in all cases would prevent many diagnostic blunders, but 
small fibroid nodules, Woolner's tip, or small sebaceous cysts should not 
be mistaken for them. Difficulty may sometimes be experienced in 
separating arthritis deformans, but the antecedent family and personal 
history and the habits of the patient, together with the absence of chalky 
deposits, serve to distinguish the one from the other disease. 

Prognosis. — The likelihood of permanent cure is not encouraging, but 
by observing proper hygienic and dietetic measures, the attacks may 
be rendered infrequent and mild, and the development of severe 
internal lesions may be postponed — whereby the gouty subject may live 
the allotted time of man. The outlook, however, is bad when gout 
develops in a young subject under thirty years, and when arteriosclerosis 
and renal changes are advanced. 

Treatment. — Attention to hygienic regulations is important. The 
patient should have plenty of fresh air; he should exercise regularly, but 
not too violently or sufficiently to cause exhaustion, since this may deter- 
mine an attack of acute gout, besides being otherwise objectionable. He 
should bathe frequently — a morning cold bath or an evening warm bath, 
as best suits the individual patient. An occasional Turkish bath, as well 
as temporary sojourns at certain spas, are often very beneficial. The 
patient should drink freely of water — to the insistence upon which the 
high repute of certain " cures" is largely due. The drinking of the water 
itself, promoting free diuresis, rather than its alkaline contents, consti- 
tutes the useful part of the treatment. The waters that enjoy the greatest 
vogue are Saratoga, Bedford, and White Sulphur, in this country; 
Carlsbad, Homburg, Ems, Kissingen, in Germany; Aix-les-Bains, 



326 DISORDERS OF METABOLISM 

Contrexeville, and Vichy, in France; and Buxton and Bath, in England. 
Sir William Roberts believes that the alkalescence of these waters is 
without influence on sodium biurate, and that the sodium salts are 
especially harmful; but since the drinking of large quantities of water 
in the solitude of one's room is a weariness to the flesh, while the same 
process at the spas not only requires considerable pecuniary outlay, but 
also promotes a healthy state of the mind, largely on account of the 
"accessories," such as regulated life, restricted diet, controlled exercise, 
baths, etc., the spas will continue to enjoy a well-merited repute. 

Since most gouty subjects eat too much, the diet must be restricted, 
but the matter of regulation of the diet is entirely individual. In general 
the meats should be reduced, and the white meats should be preferred to 
the red, though the red meats need not be prohibited. Milk and eggs 
are usually well borne and may be given in large amounts. Green vege- 
tables, such as lettuce, spinach, cauliflower, Brussel sprouts, asparagus, 
etc., are quite permissible. Though opinions differ with reference to 
carbohydrates and fats, they may be given in moderate amount. Ebstein 
favors the use of considerable butter, even in obese subjects, stating that 
not only do they improve in general condition, but actually lose some fat. 
Highly seasoned food, pastry, cheese, hot cakes and bread, tea, coffee, as 
well as liver, kidney, brain, sweetbread (rich in nuclear elements), and 
beef extracts (rich in derivatives of the xanthin group) must be prohibited. 
Sir William Roberts advises restriction of the sodium chloride of the 
food, believing that it favors the crystallization out of sodium biurate. 
In general alcohol must be strictly interdicted, especially the fermented 
beverages, such as beer, porter, ale, sweet and sour wines, champagne, 
etc. When really indicated, a small amount of whiskey or brandy, well 
diluted, may be permitted. 

During the acute attack the patient should remain at rest, preferably 
in bed, and the diet should be restricted to a minimum of milk, eggs, 
and broths. The affected member should be enveloped in cotton wool 
or hot fomentations, or a 30 to 50 per cent, ichthyol ointment, or a 
saturated solution of magnesium sulphate, and then elevated. A blue 
mass pill or a purgative dose of calomel should be administered at the 
outset. Custom sanctions the use of the wine or the tincture of colchi- 
cum in 20 to 30 minim (1.25 to 2.0 c.c.) doses, combined with potassium 
acetate or citrate, 30 to 60 grains (2 to 4 grams), every four hours, until 
the acute symptoms subside. The colchicum should be stopped imme- 
diately improvement is effected. Colchicine, T ^-g- grain (0.0006 gram) 
or more, every two or three hours, has recently been recommended as a 
substitute for the wine or the tincture. In some cases morphine may 
be necessary to relieve the pain. 

In the subacute and irregular forms of gout the salicylates have 
long enjoyed a widespread reputation and undoubtedly do good in 
many cases. In chronic cases, in addition to the foregoing measures, 
the use of potassium iodide, piperazin, guaiacum, quinine, and the bitter 
tonics, is sometimes attended by good results. The extract of thymus 
has been recommended. 



OBESITY 327 



OBESITY. 



Obesity is a disorder of metabolism characterized by the excessive 
deposition of fat in the tissues. 

Etiology. — Ordinary obesity is more common in women (especially 
Hebrews) than in men, and develops usually during the fifth decade 
(at or about the time of the menopause in women). In some cases there 
is an hereditary predisposition, in which event the obesity may develop 
during infancy, childhood, adolescence, or adult life. In the majority of 
cases the disorder is due directly to a sedentary life, indolence, deficient 
exercise, overeating, or excessive indulgence in alcohol; but especially 
to these combined. Many diseases that prevent adequate exercise, such 
as gout, chronic heart or lung disease, etc., or interfere with oxidation, 
such as anemia, etc., may lead indirectly to obesity. 

Pathology. — The lesions consist in excessive, sometimes enormous, 
deposition of fat, not only in regions where fat is found normally, as the 
subcutaneous tissues, mesentery, about the kidneys, etc., but also in 
organs normally almost, if not quite, free from fat, especially the heart, 
the liver, etc. The fatty accumulation results from imperfect metabolism 
in general — perhaps lessened vitality of the cells in general or lessened 
requirement for food to form sufficient heat and energy. The fat is 
derived from the fat and the carbohydrate (starchs and sugars) of the 
food — that amount ingested in excess of the body needs being thus stored 
up; the non-nitrogenous moiety of the proteins imperfectly oxidized also 
goes to the formation of fat. 

Symptoms. — The obvious manifestation is the excessive accumulation 
of fat in general, but especially in the chin, the back of the neck, the 
abdomen, the hips, etc. For a time, at least, there may be no symptoms 
aside from those due directly to the great bulk of tissue, and inconve- 
nience in moving it about (walking, etc.). Sooner or later, however, 
dyspnoea, especially on exertion, muscular asthenia, and other evidences 
of embarrassed cardiac action (pulmonary congestion, bronchitis, 
cyanosis, oedema, oliguria, etc.) develop, and the physical signs of fatty 
heart may be elicited. Digestion may become impaired, constipation is 
common; the liver is often enlarged; amenorrhcea, sterility, and other 
disorders may occur. Arteriosclerosis, gout, diabetes, etc., are often 
associated, and there is a special predilection to secondary infection 
(lessened resistance to bacterial infection). 

Diagnosis. — The diagnosis is easy, as a rule; myxcedema should be 
readily excluded. Other types of fatty accumulations sometimes 
must be taken into consideration, such as. (1) Adiposis dolorosa 
(Dercum), a disorder most common in middle life, in which, usually 
associated with more or less general obesity, irregular, symmetrical, 
painful, fatty masses, 1 to 3 or 4 inches in diameter (symmetrical lipo- 
matosis), develop on the trunk and extremities (but not the hands, 
feet, or face). Pain may precede the development of the fatty 



328 DISORDERS OF METABOLISM 

masses; and there may be paresthesias, anesthesias, and hyperesthe- 
sias. Asthenia, mental apathy, and psychoses may ensue. The 
disease is progressive, though of long duration, and not especially 
amenable to treatment. (2) Adiposis tuberosa simplex (Anders), a 
disorder resembling adiposis dolorosa, characterized by the develop- 
ment in the abdominal fat of fatty growths, sometimes painful to 
pressure. Unlike adiposis dolorosa, they are amenable to the ordinary 
dietetic regulations of obesity in general. (3) Adiposis cerebralis 
(dystrophia adiposo genitalis, Frohlich), a condition of marked obesity 
developing in the course of tumor of the brain (especially the pituitary 
body, pineal gland), and associated with defective development of the 
genital organs. (4) Multiple lipomatosis — multiple symmetrical fatty 
tumors occurring in association with divers diseases of the nervous 
system (tabes, general paresis, etc.). (5) Symmetrical adenolipomatosis 
(MacCormac), a condition characterized by the development of fatty 
growths (containing sclerosed lymph nodes) in the neck, axilla, etc., and 
often associated with asthenia, emaciation, rapid pulse, enlarged spleen, 
etc. The nature of these disorders is not well understood. The lesions 
found have consisted of interstitial neuritis in the fatty masses, atrophy 
and compensatory hyperplasia of the thyroid, tumors of the pituitary, 
lymphoid hyperplasia, hypoplasia or retrogression of the sexual organs, 
and divers diseases of the central nervous system. Perhaps the cases 
are much related (disorders of internal secretion). 

Prognosis. — The prognosis depends upon the nature of the under- 
lying factors and the amenability of the subject to dietetic and other 
regulations. 

Treatment. — The essence of successful treatment consists in bringing 
the diet within the requirements of the body as regards heat and energy, 
and in promoting oxidation and the destruction of fat by carefully regu~ 
lated and graduated exercise, massage, and baths — all of which must 
be carefully supervised on account of the frequency of associated cardiac 
weakness. There are several systems of dietetic regulation, of which 
the best known are Ebstein's, Oertel's, von Noorden's, and Banting's 
(for details of which one may refer to special treatises). In general, 
however, the amount of food should be reduced, especially the starches 
and sugars; the fluid intake should be greatly restricted, and the small 
amount (2 to 3 pints daily) allowed should be taken preferably two 
hours after meals than with food; alcohol should be prohibited in most 
cases. Care should be taken to see that the nitrogen output does not 
exceed the intake, since this (destruction of the body protein) is answer- 
able for most of the weakness that attends many "cures." Medicinal 
treatment is of secondary importance; a weak heart sometimes has to 
be stimulated, general weakness suggests the use of tonics, anemia 
requires the use of iron, etc. Thyroid extract is sometimes of service, 
but it must be employed with caution, since it leads to breaking down of 
the body protein as well as fat, and may induce thyroidism in those ill 
able to withstand its effects. 



RICKETS 329 

RICKETS. 

(Rachitis.) 

Rickets is a disease of infancy characterized by defective calcification 
of the growing bones and general disturbances of nutrition. 

Etiology. — Rickets occurs in the great majority of cases before the 
end of the second year of life; it is uncommon before the sixth month, 
although cases in the newborn have been described (more likely achon- 
droplasia); it is said rarely to develop about the time of puberty, 
rachitis tarda (rather osteomalacia of puberty). It is almost limited to 
the children of the poor and those who live amidst general unhygienic 
conditions; but it may occur under the best hygienic circumstances. 
Parental syphilis or tuberculosis, poor nutrition of the mother, and 
rapidly succeeding pregnancies, may be etiological factors. A faulty 
is diet the prime causative factor, whence the disease occurs in children 
fed on condensed milk, cow's milk, and proprietary foods, as well as in 
those nursed by the mother too long or when she has again become preg- 
nant. Excess of carbohydrates (deficiency of fats and animal proteins) 
is believed to be the important factor. 

Pathology. — The chief lesions occur in the bones, and consist of hyper- 
emia of the cartilage, bone marrow, periosteum, and bony tissue itself — 
which results in abnormal development of the growing bone, as well as 
changes in the bone already formed. In the long bones, ossification 
of the cartilage at the junction of the epiphysis and diaphysis is delayed 
and irregular; the outer, bluish, proliferative cartilaginous area exhibits 
irregular multiplication of the cells and a soft fibroid matrix invaded by 
bloodvessels; the inner yellowish ossifying layer becomes irregularly 
thickened and shows imperfectly calcified areas; the two layers are no 
longer sharply defined, but gradually merge. The osteoblastic layer of 
the periosteum of the shaft of the bone becomes thickened and nodular, 
the medullary cavity, continuously enlarging, results in lessening of the 
thickness of the osseous shaft. In consequence, then, of delayed and 
irregular ossification (less than one-half of the normal amount of lime 
salts may be present) the ends of the long bones are softened and nodu- 
larity enlarged and the shafts irregularly thickened — whence they readily 
become bent, distorted, or fractured. Ultimately they become ossified 
and hard, but they are likely to remain deformed. The liver, spleen, and 
mesenteric lymph nodes may become enlarged. The nature of the pro- 
cess is not well understood; it is not due to deficiency of lime salts in 
the food, nor to bacterial infection. 

Symptoms.— The onset of the disease is insidious. The early symp- 
toms, which usually develop about the time of dentition, consist, as a 
rule, of general disturbances rather than obtrusive changes in the bones, 
so that, especially among the well-to-do, the disease may be overlooked 
for some time. The child is nervous, restless, irritable, sleeps poorly, 
and may have attacks of fever; he cries when touched, seems to be 



330 DISORDERS OF METABOLISM 

generally hyperesthetic (bony prominences and soft parts), and throws 
off the bedclothes; he does not thrive, he sweats considerably, espe- 
cially about the head and neck when asleep; dentition is delayed or 
irregular; the development of the speech function is retarded; gastro- 
intestinal disturbances, such as poor appetite, vomiting, flatulence, and 
diarrhoea, are common; emaciation and anemia supervene, the muscu- 
lature becomes soft and flabby, and the child is unable to sit erect or 
walk. 

In the course of time characteristic changes appear in the bones. The 
skull is relatively large, the sutures and the fontanelles remain unclosed 
(even in the third and fourth years), and the forehead is high, wide, and 
prominent; in young infants the bones are soft and thin (craniotabes) 
and yield readily to pressure. A systolic murmur may be audible over 
the open anterior fontanelle. The costochondral junctions being swollen 
occasion the characteristic bending of the ribs (rachitic rosary), which 
usually disappears by the fourth to the sixth year; atmospheric pressure 
on the softened ribs (especially if associated with difficulty in breathing) 
may give rise to a groove along the costochondral junction, which when 
associated with a prominent sternum gives rise to the so-called pigeon 
breast or chicken breast or keel-shaped thorax; there may also be a 
groove (Harrison's) along the attachment of the diaphragm. The lower 
ends of the radius and ulna (junction of the epiphysis and diaphysis) 
become thickened, enlarged, and deformed. Similar changes may occur 
in the clavicle, the tibia (especially the lower end), and the other bones 
of the arms and legs, in the vertebrae (kyphosis, scoliosis, lordosis), and in 
the pelvis (rickety pelvis; subsequent difficulties in parturition). The 
changes in the bones of the legs (occasioning pain) and the associated 
muscular weakness lead to delay in walking, and may simulate paralysis 
(pseudoparalysis of rickets); if the child does walk, bow-leg or knock- 
knee is an almost inevitable result. Greenstick fractures of the long- 
bones are common. 

In addition, rickety children are often the subject of night terrors 
(pavor nocturnus), convulsions, tetany, laryngismus stridulus, enuresis, 
etc. The liver and spleen are often enlarged — which together with the 
marked intestinal disturbance (flatulence and muscular atony) gives 
rise to the characteristic " pot-belly." Bronchopneumonia and other 
pulmonary complications are common. 

Diagnosis. — The characteristic changes in the bones make the diagnosis 
easy; but special efforts should be made to recognize the disease early: 
open fontanelle, craniotabes, head sweating, throwing off of the bed- 
clothes, delayed dentition, and crying when touched, are important 
diagnostic-ally. Infantile scurvy (misnamed acute rickets) may be 
excluded by the aforementioned signs and symptoms, especially the 
changes in the cranium, and by the absence of the characteristic scorbutic 
changes in the gums and the bones of the legs. Syphilis may be excluded 
by the absence of other, especially cutaneous and mucous membrane, 
evidences of syphilis, and should the epiphysis be involved, by the absence 



SCURVY 33! 

of tender, painful doughy swellings, and perhaps dissociation of the 
epiphyses and diaphyses. 

Prognosis. — The disease is chronic in course, but tends to spontaneous 
recovery within a year or more; under proper treatment cure may be 
effected within several months. Deaths are usually due to complications, 
especially secondary infections. 

Treatment. — The best hygienic conditions should be procured— fresh 
air, sunlight, suitable clothing, frequent bathing, cool breezes, low 
temperature during the summer, etc. If the child is young, and the 
mother cannot satisfactorily nurse it, or if she is ill or pregnant, a wet 
nurse may be procured. Otherwise proper attention must be paid to 
the diet; cow's milk properly modified to suit the age and digestive 
abilities of the child is the best; barley water, oatmeal gruel, albumin 
water, and beef juice may be added. Phosphorus is the best remedy; it 
leads to calcium retention in rachitis, and exerts a specific effect on 
rachitic bones, increasing their calcium content; t Jq- grain (0.0006 
gram) thrice daily may be given in olive oil or cod-liver oil; and cod-liver 
oil may be rubbed into the skin. The hypophosphites, arsenic, syrup of 
iron iodide, and other iron preparations also are of service, especially in 
anemic cases. The child should not be allowed to walk until the con- 
dition is cured. 

SCURVY. 

(Scorbutus.) 

Scurvy is a chronic disorder of nutrition associated with dietetic errors 
(deprivation of fresh food), and characterized by weakness, anemia, 
spongy gums, and hemorrhages. 

Etiology. — Formerly the disease was prevalent among sailors, soldiers, 
miners, prisoners, and others deprived for a long time of fresh food; 
at present it is rare, but occasionally seen in seaports, in famine-stricken 
districts, and among the poor. Epidemics have been observed. Un- 
hygienic conditions, debilitating influences, exposure to wet and cold 
are believed to be predisposing factors; but the chief factor is in some 
way connected with the prolonged lack of fresh food, especially of fresh 
meat and vegetables; that is, it follows a diet consisting largely of dried 
or salt meat, dried vegetables, cereals, etc. Infantile scurvy (Barlow's 
disease, incorrectly called acute rickets) occurs among the well-to-do 
as well as among the poor, but in artificially fed infants, those fed on 
condensed milk, sterilized milk, proprietary food, etc. The ultimate 
etiological factor has not been determined; it is believed to be due to 
deficiency of potassium salts, especially the citrate, but also the tartrate 
and maltate (Buzzard); and to diminished alkalinity of the blood from 
an insufficient supply of vegetable salts (Rolfe). Recently Wright has 
contended that the condition is an acid intoxication due to an excess 
of foodstuffs yielding an acid ash after incineration. These, which he 
calls scorbutic, are oats, barley, fresh meats, salt meats, ship biscuit, 
wheat, eggs, rice, maize, peas, and beans; the neutral or non-scorbutic 



332 DISORDERS OF METABOLISM 

foodstuffs comprise sugar, vegetable oils, and animal fat; and the 
alkaline or antiscorbutic foodstuffs comprise carrots, turnips, potatoes, 
onions, milk, blood or meat containing blood, lime juice, orange juice, 
wood, and green herbage. Hoist contends that the disease is not an acid 
intoxication, but is due to the lack in the food of some unidentified but 
easily decomposable constituents (perhaps of the nature of an enzyme) 
— present in antiscorbutic foods, but lacking in cereals (flour, grains), 
because they are dry. 

Pathology. — The chief lesions are hemorrhagic in nature: ecchymoses 
in and beneath the skin and mucous (sometimes also the serous) mem- 
branes ; larger intermuscular and sometimes intra-articular hemorrhages ; 
subperiosteal hemorrhages (most common about the femur, but also 
elsewhere, as beneath the alveolar periosteum, etc.); and hemorrhages 
into the epiphyseo-diaphyseal junction of the long bones, associated with 
the deposition of fibrillated or reticular tissue which may soften and lead 
to separation of the epiphyses and diaphyses (which, however, may be 
retained in position by the periosteum). There may be some absorption 
of lime salts or decalcification (acidosis) and consequent fragility and 
ready fracturing. The gums become swollen, spongy, hemorrhagic, and 
sometimes ulcerated, and the teeth may become loosened. Ulcerations 
may develop in the ileum and colon. The spleen may be enlarged and 
the liver, kidneys, and heart reveal the usual results of marked anemia 
(parenchymatous and fatty degeneration). 

Symptoms. — The onset is insidious, the early symptoms consisting 
usually of general ill health, weakness, anemia, and loss of flesh. The 
hemorrhagic manifestations usually begin in the gums, which (often 
first about the canine teeth) become soft, swollen, spongy, hemorrhagic, 
and perhaps ulcerated; the teeth may fall out; the breath is very offen- 
sive, and the adjacent lymph, nodes become swollen. Petechia? and 
ecchymoses develop in and beneath the skin, especially of the legs; 
larger hemorrhages may develop in and between the muscles, especially 
of the calves, thighs, buttocks, abdominal wall, shoulder, etc. (scurvy 
induration or sclerosis); or beneath the periosteum, especially of the 
femur (painful nodular protuberances). Epistaxis, gastro-intestinal 
hemorrhage, hematuria, and other mucous membrane bleedings, and 
serous membrane hemorrhages (especially into the larger joints) may 
occur; parenchymatous (visceral) hemorrhages are rare. The hemor- 
rhagic effusions, as a rule, become absorbed, but may break down into 
foul ulcerations. There may be erythematous, urticarial, and other skin 
eruptions. Cardiovascular and pulmonary symptoms of anemia (dysp- 
noea, palpitation of the heart, oedema, etc.); headache, mental depres- 
sion and apathy, or delirium, etc., may supervene. The total acidity of 
the gastric juice is usually lessened, and the free HC1 may be entirely 
absent. Necrosis, fracture, epiphyseal separation of the bones (femur, 
clavicle, ribs) may occur. Usually there is constipation, but there may 
be diarrhoea (scorbutic dysentery). The temperature is usually normal 
or subnormal (in the absence of complications). 



SCURVY 333 

Diagnosis. — The diagnosis is easy from a knowledge of the etiological 
factors (especially in the event of epidemics), the gingival sponginess 
and hemorrhage, deep-seated intramuscular and subperiosteal hemor- 
rhages, especially in the legs, and speedy cure under the influence 
of an antiscorbutic diet. These serve to exclude purpura and hemo- 
philia. 

Infantile scurvy (Barlow's disease, formerly incorrectly described as 
acute rickets) is quite the same as the disease in the adult. In the be- 
ginning there is usually at least some slight wasting or obviously impaired 
nutrition, apathy, disinclination to movement, and general irritability. 
Soon the child is observed to cry when disturbed or touched (especially 
the lower limbs) ; pseudoparalysis of the legs seems to have developed, 
and an irregular, painful, and tender swelling of one or both thighs, 
beginning above the epiphyses, becomes apparent (subperiosteal hemor- 
rhage). Similar phenomena may develop elsewhere — in the vertebrae, 
the scapulae, the bones of the arms, etc., and the process shows a tendency 
to become symmetrical. The epiphyses may become separated from the 
shafts of the long bones (femur, costal cartilages, etc.), and crepitus may 
be elicited. Swelling of the gums (if the child has teeth), and other 
mucous membrane, cutaneous, and intermuscular hemorrhages may 
supervene; hematuria may be the only noteworthy symptom. (Edema 
of the eyelids associated with ecchymosis of the lids or conjunctiva is not 
infrequent. Asthenia is usually marked ; anemia and pallor are moderate ; 
there may be slight fever (101° to 102°). Rickets may be excluded by 
the tender painful swellings of the shafts of the bones, especially of the 
legs, and the sponginess and hemorrhage of the gums. Rickets is some- 
times believed to be associated with scurvy (scurvy-rickets); perhaps it 
predisposes to scurvy. 

Prognosis. — The prognosis is good if the disease is recognized and the 
proper treatment is instituted. In neglected cases death may ensue from 
hemorrhage, asthenia, anemia, secondary infections, etc. 

Treatment. — Nowadays the supplying of sailors, soldiers, and others 
with a suitable antiscorbutic diet effectually prevents the disease. When 
the disease has developed, a generous supply of fresh meat, fresh vege- 
tables, and the juice of two or three lemons, oranges, or limes daily 
(sweetened if desired) commonly lead to cure. If the gums are much 
swollen the diet should, be liquid or semisolid for a time; the gums 
should be painted with silver nitrate (2 to 5 per cent.); and boric- 
acid (3 per cent.), or the solutions mentioned on page 51, should be 
used as a mouth wash. Hydrochloric acid, stomachics, bitter tonics, 
strychnine, alcohol, iron, etc., are sometimes required for obvious indi- 
cations. Children should be given mother's milk if possible, or fresh 
unsterilized cow's milk suitably modified, and orange juice or lemon 
juice, other fruit juices, and meat juice, perhaps with mashed potatoes 
and vegetable purees. Iron, arsenic, cod-liver oil, brandy, etc., are 
useful adjuvants. In the event of separation of the epiphyses, splints 
should be applied. 



334 DISORDERS OF METABOLISM 

AMYLOIDOSIS. 

(Amyloid Disease; Lardaceous Disease; Waxy or Bacony Degeneration.) 

Amyloidosis is a disorder of metabolism that develops in the course of 
prolonged suppuration, especially tuberculous or syphilitic disease of the 
bones, and is characterized by the formation in the tissues and organs 
of lardacein, a combination of chondroitin-sulphuric acid and a protein. 

Etiology. — Amyloidosis follows prolonged suppuration and long- 
continued loss of the body proteins. It is most common in advanced 
tuberculosis, especially of the bones and joints (Pott's disease of the 
vertebrae, hip disease, etc.); it occurs also in advanced syphilis, some- 
times even in the absence of suppuration; in non-tuberculous and non- 
syphilitic suppurative processes, such as osteomyelitis, empyema, etc.; 
in non-suppurative disorders leading to anemia and cachexia, such as 
malaria, leukemia, carcinoma, chronic nephritis, prolonged lactation, 
etc. ; and sometimes it occurs without obvious cause. The disorder is 
most common in young adults (before the fortieth year), and in males, 
since they are more subject than females to the initiating causes. 

Pathology. — The lesions are sometimes confined to a single organ; 
usually they are widespread, being most common in the kidneys, spleen, 
and liver (which often are involved concurrently) ; they occur also in the 
small intestine, the lymph nodes, the adrenals, the stomach, the large 
intestine, the heart, the pancreas, the thyroid, the bone-marrow, etc. 
The solid viscera become enlarged, firm, dense, and heavy; they take on 
a homogenous, semitranslucent or wax-like appearance, and give a 
characteristic reaction with iodine and other substances. The lardacein 
is not, as was formerly supposed, an infiltration derived from the blood, 
but is a formation developed in situ in consequence of an interaction 
between chondroitin-sulphuric acid brought by the blood or the lymph- 
atics and the local protein; the process is in some way determined or 
influenced by bacterial (and perhaps other) toxins, notably the toxins of 
staphylococci, streptococci, etc. The suppurative processes in which 
amyloidosis occurs are in most instances examples of secondary pyo- 
coccic infections. The amyloid material is deposited in the outer sur- 
face of the capillary vessels, and in the intima and media of the arteri- 
oles; the adventitia is rarely, and the endothelium never, affected. In 
the kidneys the Malpighian tufts are especially involved, in the liver the 
midzonal region of the lobules, in the spleen the Malpighian bodies, and 
in the mucous membranes tke arterioles. 

Symptoms. — The symptoms are largely those of the antecedent dis- 
order, of which the amyloidosis is the end result. With gradual increase 
in the anemia, cachexia, and weakness, the abdomen is observed to 
enlarge, or polyuria, diarrhoea, or oedema may develop. The abdominal 
enlargement is readily found to be due to enlargement of the liver or 
spleen or both; the liver may become enormous, and is smooth, hard, 
firm, and has a somewhat sharp or rounded edge; the spleen is enlarged 



INFANTILISM 335 

and presents a firm, resisting, blunt edge. There is rarely any jaundice, 
and ascites develops only as part of anasarca. Involvement of the kid- 
ney is shown in oedema and increase in the amount of the urine, which 
is pale in color and of very low specific gravity; it contains usually a 
considerable amount (sometimes very little) albumin, and hyaline and 
waxy casts (which may give the amyloid reaction). In the event of 
associated nephritis (which is common) cellular casts, arterial hyper- 
tension, arteriosclerosis, hypertrophy of the heart, retinal changes, etc., 
may be found. Involvement of the intestine may be symptomless, but 
if advanced, the lesions are likely to be disclosed by more or less intract- 
able and painless diarrhoea. Changes in the cutaneous vessels, and a 
failing heart, are often in part answerable for the oedema. 

Diagnosis. — The diagnosis is readily made, the combination of the 
etiological factor, progressive increase of anemia, cachexia, and weak- 
ness, enlargement of the liver and the spleen polyuria, albuminuria, and 
diarrhoea being unmistakable. 

Prognosis. — The prognosis depends chiefly on the initiating cause; the 
advent of the amyloidosis only makes the prognosis hopeless. 

Treatment. — The treatment is wholly that of the primary disorder. 



INFANTILISM. 

Infantilism is a condition characterized by the persistence beyond the 
ordinary age of puberty of the physical and mental attributes of child- 
hood, including hypoplasia of the sexual organs and absence or abeyance 
of the secondary sexual characteristics. The individual remains a child 
in body and in mind (emotions and intelligence), the adult bodily char- 
acteristics remain in abeyance or become ill developed, the union of the 
epiphyses and diaphyses of the long bones fails or is much delayed. In 
the male, the facial, axillary, and pubic hair does not grow, nor does the 
larynx enlarge or the voice deepen; in the female, the axillary and pubic 
hair does not grow, the breasts do not develop, the hips do not widen, and 
there is little indication of the female waist. The underlying causes may 
be present at birth (congenital cases); or the condition may be due to 
factors that become operative in early or late childhood. The ensuing 
phenomena vary accordingly: in some the infantilism is complete, in 
some incomplete, whereas in other, perhaps related, cases the onset of 
puberty is merely delayed — full and normal development ultimately 
ensuing. Several types may be distinguished : 

The Lorain Type.— In this, beyond the ordinary age of puberty, 
the figure remains small and childlike as regards height, but the general 
contour is that of approaching puberty. Although there is no growth of 
the facial, pubic, or axillary hair, nor of the breasts in the female, the gen i- 
tal organs are well formed, although small; the head is relatively small, 
the shoulders are fairly broad, and the bony prominences and muscles are 
distinct — a miniature man or woman who has retained the characteristics 



336 DISORDERS OF METABOLISM 

(mental as well as physical) of childhood. The cause of the disease is not 
known: indeed, it is sometimes referred to as idiopathic; but syphilis, alco- 
holism, and consanguinity in the parents are believed to be of etiological 
importance; and defective development of the cardiovascular system is 
believed to be the main factor. 

The Cardiac Type. — Congenital heart disease, and also heart dis- 
ease beginning early in life, especially pulmonary or aortic stenosis, may 
lead to infantilism. In some otherwise fairly normal, although small 
adult individuals a concealed or latent mitral stenosis may be found. 

The Metabolic Type. — Disorders of internal secretion apparently 
may give rise to several varieties of infantilism. Thyroid inadequacy, 
congenital or developing early in life, occasions a so-called myxcedema- 
tous infantilism or cretinism (Brissaud's type; Hertoghe's hypothyroid- 
ism), which may be cured by thyroid extract. Another form occurs in con- 
nection with disease of the pituitary : hyperpituitarism originating in youth 
gives rise to gigantism, which may be associated with infantile proportion 
of the body, infantile genital organs, delayed union of the epiphyses and 
diaphyses, etc. Hypopituitarism originating in youth gives probably 
rise to infantilism of mind as well as body. Gilford's cases of dwarfs, 
micromegaly, ateliosis (continuous youth and premature old age), or 
progeria perhaps belong to this category. A pancreatic form, sup- 
posedly due to deficient pancreatic secretion and associated with recur- 
ring attacks of severe diarrhoea in children, has been described by Byron 
Bramwell. Improvement has followed the use of pancreatic preparations. 

The Intestinal Type. — Herter describes as intestinal infantilism a 
condition occurring in childhood, and characterized by arrest in the 
development of the body (skeleton, muscles, and organs), maintenance 
of good mental powers and fair development of the brain, marked 
abdominal distention, slight, moderate, or considerable degree of simple 
anemia, the rapid onset of physical and mental fatigue, irregularities of 
intestinal digestion resulting in frequent diarrhceal discharges, excessive 
appetite, various minor signs of nervous instability, subnormal tempera- 
ture, cold hands and feet, and slight signs of rickets. Indol and phenol 
compounds occur in the urine; fat absorption is impaired; and the 
resorption of calcium and magnesium is deficient. Herter attributes the 
condition to the overgrowth and persistence of the bacterial flora of the 
intestine belonging normally to the nursling period (Bacillus bifidus and 
Bacillus infantilis). The condition is persistent, and relapses are com- 
mon; some of the children die of acute intestinal infections; others are 
likely to be permanently dwarfed; but normal growth may follow 
careful dietetic regulations. 



SECTION IV. 

DISEASES OF THE DUCTLESS GLANDS AND 
OF INTEENAL SECRETION. 



Pathological Physiology. — In addition to the several organs, such 
as the stomach, the liver, the pancreas, the kidneys, the testicle, etc., 
which produce a secretion that can be readily procured and studied, 
other organs produce a secretion not so open to investigation, a secretion 
which, since it is not discharged through the medium of a duct from the 
organ that produces it, is spoken of as an internal secretion, and the 
organ in question as a ductless gland. In a certain sense all of the body 
cells produce an internal secretion — the result of their metabolic activity 
— which they give off into the lymph or blood stream. Some of these are 
the end results of destructive metabolism and of no further use in the 
economy — indeed, they may be distinctly harmful if not excreted (cer- 
tain forms of auto-intoxication); others are more or less essential to the 
orderly performance of the functions of other organs, necessary to the 
preservation of life and the maintenance of health ; these are the internal 
secretions in a restricted sense, and the "glands" that produce them are 
the "ductless glands" or the glands with an internal secretion. They 
comprise especially the thyroid, the parathyroids, the adrenals (and the 
chromaffin system), and the pituitary body, which are endowed with 
specific functions that will be discussed under the respective headings; 
perhaps the carotid and coccygeal glands also should be here included, 
but nothing is known of their function. But other organs produce 
internal secretions: some of these also are "external secretion;" thus, the 
pancreas pours into the duodenum a secretion that contains tripsinogen, 
which hydrolyzes protein, diastase (amylase), which hydrolyzes carbo- 
hydrates, lipase (steapsin), which saponifies and indirectly emulsifies 
fats, and perhaps other enzymes (rennin, lactase, etc.); but, in addition, 
the islands of Langerhans of the pancreas, which are not in communica- 
tion with the pancreatic duct, produce an internal secretion that finds 
its way directly into the blood and controls the katabolism of the dextrose 
of the blood, muscles, and other tissues— a subject discussed under 
diabetes. The liver and the kidneys, in a certain sense, also have an 
internal secretion in addition to the more obvious external secretion— 

22 



338 DISEASES OF THE DUCTLESS GLANDS 

the bile and the urine. The liver, by a process that may be described as 
internal secretion, produces glycogen and an enzyme (urease) that leads 
to formation of urea from protein derivatives; and the kidneys appear also 
to produce a proteolytic enzyme subserving the same purpose, though 
probably acting in the liver or the muscles rather than in the kidney 
itself. The testicle and the ovaries, in addition to their specific secretions 
which are discharged externally, produce also an internal secretion 
which is credited with the production of the secondary male and female 
characteristics respectively, and seems to exercise some tonic influence 
on the neuromuscular system. Castration in either sex results in lessened 
oxidation, accumulation of fat, and in more or less loss of the secondary 
sexual characteristics, which loss may be prevented or retarded by the 
use of testicular or ovarian preparations respectively. The duodenum 
produces secretin which stimulates the pancreas to activity and entero- 
kinase which activates the proteolytic ferment of the pancreatic juice 
(trypsinogen) ; but these can scarcely be called internal secretions in a 
restricted sense. Organic substances subserving such a stimulating 
purpose have recently been spoken of as kinases, while similar inor- 
ganic substances have been called activators. The spleen, the lymph 
nodes, the hemolymph nodes, and the thymus also, perhaps, produce an 
internal secretion, but there is no conclusive evidence of the fact; their 
diseases are discussed under diseases of the blood and hemopoietic 
system. 

The ductless glands, or the glands with an internal secretion in a 
restricted sense, are subject to many complicated and ill-understood 
relationships; thus, in diseased states at least, there is a more or less 
marked relationship between the thyroid and the pituitary, between the 
thyroid and the thymus, between the pituitary and the testicles and the 
ovaries, and between the thyroid, the pancreas, and the adrenals. The 
functional harmony of these organs is maintained and their correlated 
interaction is effected through the medium of chemical substances, so- 
called hormones, that circulate in the blood and other fluids of the body. 
Whereas, the pancreas and the thyroid, and the pancreas and the adrenals 
(and the chromaffin system) each inhibits the metabolic activities of the 
other, the thyroid and the adrenals (and the chromaffin system) seem 
the one to augment the activities of the other. Experimental removal 
of one of these glands not only results directly in a loss of its functional 
activities, but leads also indirectly, since restraint is removed, to an in- 
creased or diminished functional activity of the correspondingly related 
gland; and augmented functional activity (such as may be attained by 
feeding experiments or the injection of active principles or extracts) has 
a contrary effect. Thus, for instance, loss or diminution of the internal 
secretion of the pancreas, in consequence of the corresponding loss of 
inhibition, is associated with hyperfunction of the thyroid (increase of 
protein metabolism) and of the adrenals and the chromaffin system 
(adrenal glycosuria). Similar phenomena occur also in human subjects: 
thus, hyperthyroidism is sometimes associated with alimentary glycosuria 



DISEASES OF THE THYROID GLAND 339 

or diabetes. The pigmentation of Graves' disease (resembling that of 
Addison's disease) suggests a relationship between the thyroid and the 
adrenals. There are many other evidences of mutual inter-relationship 
between the ductless glands, which, however, are ill understood. 



DISEASES OF THE THYEOID GLAND. 

Pathological Physiology— The normal physiology of the thyroid is 
ill understood. In consequence of the activity of its specific principle 
iodothyrin (a constituent of colloid and not found elsewhere in the 
body), and perhaps also of other unknown principles, it exercises a 
profound influence on metabolism. It detoxifies intermediate products 
of metabolism or gives over into the circulation an internal secretion 
essential to the normal functional activity of other organs, acting, there- 
fore, as a hormone and seeming to have a specific action on the central 
and the sympathetic nervous systems and on the skin and the subcutane- 
ous tissues. Injection of thyroid preparations increases protein and fat 
katabolism. An influence of deficiency of secretion on carbohydrate 
metabolism is evident in the fact that after thyroidectomy injections of 
adrenalin do not cause glycosuria; that is, the limits of carbohydrate 
metabolism are increased. Deficiency of secretion also exercises a restrain- 
ing influence on the healing of fractures; an excess seems to accelerate the 
healing. Destruction or loss of function of the thyroid (athyrea, hypo- 
thyroidism) results in congenital or acquired myxctdema; and an excess 
of function (hyperthyroidism), or perversion of function (dysthyreosis), 
is the basis of Graves' disease; whence the two diseases represent the 
one the antithesis of the other. In the one the gland is atrophic or 
absent, in the other hyperplastic and hyperactive; in the one metabolism 
is deficient and the patient increases in weight, in the other metabolism 
(especially the consumption of oxygen) is augmented and the patient 
usually emaciates; in the one the patient is dull, apathetic, and mentally 
deficient, in the other nervous and highly excitable; in the one the skin is 
dry, thick, cool, and inactive, in the other moist, warm, and active (ery- 
thema, flushing, sweating); in the one the temperature is low, the pulse 
is slow, and the urine lessened, in the other the temperature is increased, 
the pulse is rapid (tachydcardia), and the urine increased; in the one 
(which may result from excision of the thyroid) the symptoms may be 
ameliorated or the condition entirely cured by the use of thyroid extract, in 
the other, symptoms are made worse by thyroid extract — which may also 
provoke similar phenomena in normal individuals — and the condition 
may be benefited or cured by partial thyroidectomy. 

Thyroid preparations have been used with some success in certain 
disorders of metabolism, such as obesity, arthritis deformans, etc. 
Their use, in obesity, for instance, in which they seem especially indicated 
to augment the katabolism of fat, is not without danger, since although 
they have a much greater accelerative influence on protein katabolism, 



340 DISEASES OF THE THYROID GLAND 

they may cause glycosuria or diabetes (which is often latent in obese 
subjects), and a fatty heart may not be able well to maintain the provoked 
increased activity. 

ACUTE THYROIDITIS. 

Etiology. — Acute inflammation of the thyroid occasionally occurs, 
usually in young subjects, in consequence of trauma or of bacterial 
infection. The infectious cases are rarely primary; usually they are 
secondary, occurring in the course of typhoid fever, scarlatina, diphtheria, 
measles, influenza, smallpox, some cases of recent syphilis, etc. The 
lesions may be simple or purulent. 

Symptoms. — The symptoms consist of local pain and tenderness, sen- 
sation of fulness in the neck, perhaps difficulty in swallowing, and an 
enlarged and more or less tender thyroid. In the event of suppuration 
a local area of softening or fluctuation may be detected. The general 
symptoms are those of the primary infection, augmented perhaps by the 
local inflammation. 

Diagnosis- -In the diagnosis one must exclude simple congestion, 
such as occurs especially in women from emotional excitement, disturb- 
ance of the sexual organs, interference with the circulation (tight collars), 
etc. 

Prognosis. — The prognosis, as a rule, is good as regards the thyroiditis 
itself, but modifications in the gland may lead later to Graves' disease 
or myxcedema. 

Treatment. — The treatment is that of the primary disorder, with local 
antiphlogistic measures (especially an icebag), and incision in the event 
of suppuration. 

GOITRE. 

(Simple Goitre; Struma; Bronchocele.) 

Goitre is a term indiscriminately applied to any enlargement of the 
thyroid gland. It is often qualified by the terms benign and malignant 
(comprising the tumor formations); and a simple goitre is differentiated 
from the so-called exophthalmic goitre. 

Etiology. — Simple goitre occurs as a sporadic, an endemic, or an epi- 
demic disease. The sporadic disease occurs in all parts of the world. 
The disease is endemic especially in the Swiss and Italian Alps, but also 
in certain regions of France, Spain, Germany, England, Asia, and in our 
own country in the region of the great lakes; in these endemic regions 
small epidemics sometimes occur from time to time, as well as occasion- 
ally in barracks, schools, etc. The disorder is more common in women 
than in men (six or more to one). It is sometimes congenital. The 
goitre begins to develop usually at puberty or soon thereafter, and may 
continue to increase in size throughout life, although, attaining a consid- 
erable size by the time adult life is reached, it may remain stationary. 



GOITRE 341 

The cause of the disease is not known, although it has been attributed to 
the water, air, and soil of endemic centres; special significance has been 
attributed to the drinking-water — mineral, radio-active, and bacterial 
constituents. 

Pathology.— The thyroid is more or less enlarged, either uniformly 
or one lobe more than the other; the shape of the organ is generally 
more or less preserved; the enlargement is often nodular, although it 
may be smooth. On section it resembles the normal gland, although 
often the colloid is obviously increased. Parenchymatous (or colloid), 
cystic, and vascular goitres are sometimes distinguished. Hyaline degen- 
eration, calcareous infiltration, and fibrosis are not uncommon in ad- 
vanced cases. MacCarthy differentiates the following types or stages 
of goitre: (1) Cystic goitre (usually spoken of as simple or colloid 
goitre), composed of many small and large cysts with colloid contents; it 
leads to enlargement, but no symptoms other than those due to press- 
ure. (2) Hypertrophic parenchymatous goitre — hypertrophy of the 
parenchyma with little or no cyst formation. (3) Papillary cystic 
goitre— cyst formations with colloid contents, papillary ingrowths into the 
alveoli, or cysts with consequent increased secreting surface. Hyper- 
thyroidism may occur in types 2 and 3. (4) Hypertrophic fcetal thyroid 
— a small amount of epithelial tissue and a great amount of inter- 
glandular connective tissue — the goitre of the cretin with tumor formation 
and hypothyroidism. (5) Fcetal adenoma or adenomatous hypertrophy 
of the fcetal thyroid, instead of connective tissue overgrowth; it may occur 
as an encapsulated tumor, occasioning inconvenience only by pressure, 
or degenerative or circulatory changes may occur and lead to hyper- 
thyroidism. 

Symptoms.— The chief symptom is the goitre itself, which may be 
very small or very large, and involve the entire gland, or one lobe only 
or disproportionately, or the isthmus; it may grow larger behind the 
sternum or the clavicles. When large it may lead to inconvenience on 
account of its size and weight, or it may cause compression phenomena 
— on the trachea, oesophagus, arteries, veins, and nerves of the neck. 
Sudden death occasionally occurs in large goitres from pressure on 
the vagus, hemorrhage and compression of the trachea, oedema of the 
glottis, etc. 

Diagnosis. — The diagnosis, as a rule, is obvious; one must exclude 
tumors and exophthalmic goitre. 

Prognosis. — The condition is essentially chronic, although some cases, 
so-called acute goitres, that develop in newcomers into an infected 
region, often disappear if the subject soon leaves. The prognosis is 
influenced by the size and direction of growth and the presence or absence 
of compression phenomena. 

Treatment.— Boiling the drinking-water in goitrous regions is usually 
advised as a prophylactic measure. Change of residence to a non- 
goitrous region is much preferable. Counterirritants, iodine externally, 
and the iodides and ergot internally, and the rr-rays locally are sonic- 



342 DISEASES OF THE THYROID GLAND 

times of service, especially if the goitre be small and of recent develop- 
ment. Large and growing goitres should be treated surgically — removed 
in part. 

HYPERTHYROIDISM AND EXOPHTHALMIC GOITRE. 

(Gloves' Disease; Basedow's Disease; Parry's Disease; Flajani's Disease.) 

Exophthalmic goitre is a condition of aggravated hyperthyroidism, 
characterized by enlargement of the thyroid, exophthalmos, tachycardia, 
muscular tremor, and vasomotor disturbances; it takes its name from 
the two obtrusive manifestations of the disorder, but there are many 
more or less ill-developed cases that present neither goitre nor exoph- 
thalmos and are preferably spoken of as hyperthyroidism. 

Etiology. — From 80 to 95 per cent, of the cases occur in women, and 
most frequently between the ages of fifteen and thirty years. The 
disease is rare during childhood, but is not uncommon in the fourth 
decade. The cause is not known; it develops not uncommonly at 
or shortly after puberty; its onset is sometimes attributed to fright, 
fear, excitement, worry, anemia, chlorosis, gastro-intestinal disturbances, 
infections, etc. Perhaps these factors, if at all operative, are to be 
interpreted as furnishing nervous, toxic, infectious, or metabolic stimula- 
tion to the thyroid. Etiological significance is sometimes attributed to 
locality and climate, but the nature of the relationship, if any, is not 
understood. 

Pathology. — The significant lesion consists of enlargement of the 
thyroid, which varies considerably in different cases; it may be very 
slight or very great, symmetrical or asymmetrical, firm or soft and 
elastic (parenchymatous, fibrous, or cystic). The characteristic micro- 
scopic lesions consist of changes in the size and configuration of the 
alveoli, due especially to hyperplasia and infolding of the epithelium; 
increase in the size of the epithelial cells — the normal low cuboidal 
cells giving way to high cylindrical cells ; and gradual disappearance and 
absorption of the colloid material; with these there is also associated 
an increase in the bloodvessels and the connective tissue stroma. The 
symptoms are attributed to thyroid toxemia due to the absorption of 
the products of a hyperactive (perhaps perverted) thyroid (hyperthyroid- 
ism) ; this consists in part of iodothyrin, a constitutent of the colloid, 
which is usually lessened in the exophthalmic goitres; perhaps also to 
other unknown substances. Sometimes lesions are found in the central 
nervous system (especially the restiform bodies of the medulla), and in 
the sympathetic nervous system (especially the cervical sympathetic) ; but 
they are inconstant and probably not significant. The muscles, despite 
the tremor, show no noteworthy lesions aside from some atrophy, espe- 
cially of the muscles of the neck, hand, arms, and peroneus; in advanced 
cases the heart becomes hypertrophied, dilated, and degenerated. 

Symptoms. — The onset, as a rule, is insidious, the symptoms mild, 
moderate, or severe, and the course protracted — chronic cases; occa- 



HYPERTHYROIDISM AND EXOPHTHALMIC GOITRE 343 

sionally the onset is abrupt — acute cases, which also may be mild, 
moderate, or severe; the severe cases may run a rapid course and soon 
lead to death. In some cases the symptoms of hyperthyroidism are 
present from the beginning (primary cases), whereas in others they 
supervene upon a goitre already, perhaps for a long time, existent 
(secondary cases). In some cases the symptoms are many and obtru- 
sive (outspoken or complete cases), whereas in others they are few, 
irregular, atypical (incomplete, rudimentary cases, formes frustes of the 
French). Remissions and exacerbations are common. 

The characteristic features of the disease consist of enlargement 
of the thyroid, exophthalmos and other ocular symptoms, tachycardia, 
muscular tremors, and various vasomotor disturbances. The goitre is 
almost invariably present, some enlargement being present in many 
cases in which it is not suspected; but there is no relationship between 
the size of the goitre and the severity of the symptoms; it is often 
present from the beginning, but sometimes it develops later, at least 
in an obtrusive form. It may be slight, moderate, or extreme, and 
vary in size from time to time (during menstruation, pregnancy, times of 
worry, etc.); it may be unilateral, bilateral, symmetrical or asymmetrical; 
firm or soft, elastic, and semifluctuating. It is rarely painful except 
when acutely enlarged (vascular enlargement), and unless very large 
gives rise to no noteworthy signs of compression of the trachea or 
adjacent organs. It may pulsate, and on ausculation reveal a systolic 
(arterial) and sometimes also a diastolic (venous) murmur. 

Exophthalmos is present in from 75 to 90 per cent, of the cases, and 
although a very obtrusive symptom, is not, as a rule, an early symptom. 
It varies much in degree (25 to 30 millimeters, as measured by the 
Hertel exophthalmometer, the normal being about 20 millimeters in 
adults, and less in children); ordinarily it just about prevents com- 
plete closure of the eyelids, but rarely the eyeballs may be advanced 
altogether beyond the eyelids. Usually it is bilateral, although unequal; 
it may be almost if not completely unilateral, and perhaps associated 
with homolateral goitre. There are a number of associated ocular phe- 
nomena: A peculiar staring expression (widening of the palpebral fissure), 
the whites of the sclera? showing all around the cornea (Dalrymple's 
sign), associated with infrequent and incomplete reflex winking (Stell- 
wag's sign); lagging of the upper eyelids in downward movement of 
the eyeballs — incoordination in the movements of the eyelids and the 
eyeballs (von Graefe's sign); lack of the power of binocular convergence 
unassociated w T ith diplopia (Moebius' sign); difficulty or inability to 
evert the upper lid (GifTord's sign); tremor of the upper lid when it 
has been closed gently (Rosenbach's sign) ; sudden elevation of the upper 
lid, exposing the sclera, if the patient looking straight forward is directed 
quickly to look upward; that is, the lids contract spastically in advance 
of the elevating eyeball (Kocher's sign). All of these eye signs, including 
the exophthalmos, are due to toxic contraction of the unstriped orbital 
muscle arising from the orbital septum anteriorly and inserted just 



344 DISEASES OF THE THYROID GLAND 

posterior to the equator of the eyeball, and spasm of the unstriped superior 
and inferior tarsal muscles of Miiller; vascular engorgement and oedema 
of the orbital cavity also have been looked upon as causes. There may 
also be absence of wrinkling of the forehead when the patient looks 
upward (Joffroy's sign); a sensation of tension or strain in or behind 
the eyeballs; tremor of the eyeballs; paralyses of the ocular muscles; 
excessive dryness or epiphoria; retinal, pupillary, or corneal (ulcerative) 
changes; pigmentation of the eyelids (Tellais' sign), etc. 

Tachycardia is always present, and is commonly the earliest note- 
worthy manifestation. The pulse is usually above 100, and not infre- 
quently 160 to 180 or more. There is associated palpitation and over- 
action of the heart, throbbing of the peripheral arteries, especially of 
the neck, a capillary (and perhaps a venous) pulse, early a functional 
systolic murmur, later evidences of hypertrophy and dilatation of the 
heart (especially of the left ventricle), with relative mitral insufficiency, 
arrhythmia, etc. Hemorrhages, especially epistaxis, but also hemoptysis, 
hematemesis, etc., sometimes occur. Muscular tremors, fine, rhythmic, 
8 to 10 to the second, are present in almost all cases and are noteworthy 
in more than one-half of the cases. There is often also marked mus- 
cular weakness; sometimes a peculiar giving way of the legs (Charcot). 

There are many vasomotor symptoms, such as subjective complaint 
of warmth, and itching, dermographism, erythema, urticaria, angio- 
neurotic oedema, readily provoked and excessive flushing and sweating, 
diarrhoea, sometimes vomiting and abdominal pain, periodical polyuria, 
cough, dyspnoea, intermittent (sometimes painful) swelling of the joints, 
etc. Often there are nervous symptoms, such as headache, vertigo, 
insomnia, different forms of paralysis, mental irritability or depression; 
occasionally, especially in the acute cases, psychoses. The skin reveals 
lessened resistance to the galvanic current (Chvostek); it may become 
pigmented or reveal spots of vitiligo; the hair may fall. Attacks of 
fever, remittent or intermittent, lasting several days or several weeks, are 
not uncommon. The metabolism is increased (excessive nitrogenous 
and other excretion). 

Eventually emaciation, cardiac weakness (myocardial degeneration), 
low blood pressure, and more or less secondary anemia supervene. 
There may be a relative lymphocytosis (usually no leukocytosis; some- 
times leukopenia), and the coagulability of the blood may be lessened. 
Unusual and rapid loss of weight often attends acute exacerbations of 
the disease (fever, vomiting, diarrhoea, marked vasomotor disturbances, 
extreme tachycardia, arrhythmia, perhaps mania, etc.) ; the loss may be 
partly compensated for by gain during a succeeding period of remission. 
Death may ensue from acute thyroidism, cardiac weakness, exhaustion 
from vomiting and diarrhoea, secondary infection (tuberculosis, pneu- 
monia, etc.), diabetes (which sometimes ensues), etc. 

Diagnosis.— The fully developed disorder presents no diagnostic 
difficulties, but incomplete cases, slight or moderate hyperthyroidism, 
often go unrecognized. Attention to other than the three (formerly) 



HYPERTHYROIDISM AtiD EXOPHTHALMIC GOITRE 345 

so-called cardinal symptoms (goitre, exophthalmos, and tachycardia) 
will often enable one to make the diagnosis in early stages and in 
aberrant cases. Tachycardia and the vasomotor phenomena (which 
determine the severity of the disease) with or without slight tur- 
gescence of the thyroid, are of great diagnostic significance. One 
must not mistake the slight and temporary enlargement of the 
thyroid that may follow shocks and emotional disturbances, or occur 
at puberty, during pregnancy, and the climacteric, for Graves' dis- 
ease, although these may progress to the most serious disorder, and 
time alone may be required for demonstrative differentiation. Nor 
should the enlargement of anemic states, especially chlorosis, and of 
some forms of heart, especially mitral, disease be mistaken. The 
hyperthyroidism of early tuberculosis (sometimes associated with tuber- 
culosis of the thyroid), neurasthenic states in which transitory thyroid 
enlargement is not uncommon, etc., must also be excluded. In doubtful 
cases recourse may be had to the use of iodine internally or some 
thyroid tablet : in the event of hyperthyroidism even small doses readily 
provoke tachycardia and other characteristic symptoms (intolerance of 
the hyperthyroid subject). 

Prognosis. — The disease usually runs a protracted course, extending 
over many years — twenty or more. Spontaneous recovery in well- 
developed cases is rare; but mild cases or moderate grades of hyper- 
thyroidism may be much benefited, if not completely cured, by appro- 
priate treatment. Marked benefit, if not cure, may be expected in at 
least half of the cases. Cases that develop acutely, or acute exacerbations 
of chronic cases, may lead to death within a few weeks to a few months. 

Treatment. — Rest with freedom from care, worry, and excitement 
are of prime importance; in severe cases, rest in bed for a month or two 
is essential; and in all cases a change of scene and air is beneficial. Care- 
ful attention must be directed to the diet, so that the patient may be 
well nourished. Thomson (who believes the disease to be a toxemia 
originating in the intestinal tract) urges the use of fermented milk 
(kefir) or peptonized milk in large amounts, vegetables (except peas, 
beans, and asparagus), crusty bread, rice, and fruits (except uncooked 
apples and strawberries), and the prohibition of butcher meat, oysters, 
clams, and lobsters; one egg daily may be permitted, and a small 
amount of non-oily fish, poultry, quail, or partridge may also be 
taken. The bowels must be opened daily; paroxysms of diarrhoea 
may .require the use of astringents, which, however, are rarely very 
useful. General hydrotherapy, as well as cold applications to the 
thyroid and the heart are very useful. The cardiovascular and vaso- 
motor phenomena are perhaps best controlled with belladonna (or 
atropine) given to the point of toleration; the bromides and other 
nervines, or small doses of opium for short periods, are sometimes 
useful adjuncts, but opium should be given with the greatest circum- 
spection, or not at all, to subjects in whom the prognosis is relatively 
good. The hyperactivity of the heart is sometimes benefited by aconite 



346 DISEASES OF THE THYROID GLAND 

or veratrum viride; little benefit attends the use of digitalis, strophanthus, 
convallaria, etc., unless there is actual disease of the heart; otherwise 
arrhythmia, etc., may be made worse. A number of drugs have been 
more or less highly extolled from time to time. Arsenic is believed 
to exercise a modifying influence on the secretion of the thyroid: to 
secure results it must be given for a long time; phosphorus, especially 
in the phosphates, also is credited with some action on the thyroid secre- 
tion, but it is doubtful if, as usually given (sodium phosphate), it exercises 
any virtues other than those attending free evacuation of the bowels; 
quinine hydrobromide (the neutral salt) to the point of toleration for 
a long time is said to exert beneficial, even curative, properties. In 
addition to sodium phosphate before each meal and a blue mass pill 
twice weekly, Thomson uses intestinal antiseptics, such as sodium sali- 
cylate and sodium benzoate, of each 10 grains (0.6 gram) one hour after 
each meal, and a capsule of naphthelene 3 grains (0.2 gram) and sodium 
benzoate 6 grains (0.4 gram) at bedtime; phenol bismuth and ammo- 
nium benzoate also are used. Iron is of value in anemic subjects. Ergot, 
adrenalin, electricity, the x-rays, etc., have been advocated from time to 
time; but they are of doubtful value. Iodine, the iodides, and thyroid 
extract are, as a rule, harmful. The serum of thyroidectomized dogs, 
sheep, and goats, and the milk of thyroidectomized goats, and extract of 
the thymus, have been used in the belief that they contain specific anti- 
bodies; but great success seems not to have attended their use. The 
cytolytic serum of Rogers and Beebe seems to be definitely curative in 
some cases, but further experience in its use is desirable. Surgical treat- 
ment (resection of part of the thyroid; ligation of the superior thyroid 
arteries) is indicated in patients who do not improve under well-directed 
medical treatment, including rest, in from three to six months, in those 
who become progressively worse under medical treatment, and in those 
with signs of local pressure. 



HYPOTHYROIDISM; CRETINISM; MYX (EDEMA. 

Deficiency of the thyroid secretion (hypothyroidism, athyrea), may 
give rise to one of three conditions : (1) Cretinism; congenital or acquired 
myxcedema of infants and children; (2) spontaneous myxcedema of 
adults; and (3) postoperative myxcedema. 

Cretinism. — Cretinism is a disorder due to lack of thyroid secretion 
and characterized by imperfect development of the body and the mind. 
It occurs as an endemic and a sporadic affection. Endemic cretinism 
is common in endemic goitrous regions. One or both parents may 
be goitrous, or mildly cretinoid; although if both parents are cretins 
the marriage is usually sterile. The thyroid may be absent or small, 
sometimes normal in size or enlarged ; the epithelium is atrophic and the 
colloid is increased. Sporadic cretinism occurs in non-goitrous regions, 
and may result from aplasia or hypoplasia of the thyroid, thyroiditis (infec- 



HYPOTHYROIDISM; CRETINISM; MYXEDEMA 347 

tions with consecutive sclerosis or destruction of the thyroid parenchyma). 
The lesions are quite the same as those of endemic goitre. The thymus 
often persists. 

Symptoms. — Usually toward the end of the first or during the second 
year arrest of bodily and mental development becomes apparent (in- 
fantile form); occasionally the symptoms are delayed for several years 
(juvenile form), although they always appear before puberty; but the 
earlier the onset the more marked the phenomena. The head is large, 
the fontanelles are open, the forehead is low and broad, the nose is 
flat, the mouth is usually open, the lips are thick and through them 
protrudes a thickened tongue; the expression is stolid, idiotic, or quite 
bestial. The body is stunted, dwarfed, the limbs and the neck are short 
and thick, the skeletal muscles small and inefficient, and the gait, if the 
child walks at all, weak and waddling; and the abdomen is large and pro- 
tuberant. The skin is pallid, dry (no sweating), thick, inelastic, and 
seemingly cedematous (but does not pit on pressure — myxedematous) ; 
the hair is thin and scanty, the nails brittle, and the teeth carious. The 
body temperature is low, the pulse infrequent, and metabolism deficient. 
The child is more or less idiotic, difficult or impossible to train; speech 
is often limited to a few more or less inarticulate words ; deafness may be 
present; the genitals are retarded or do not develop at all. Cretins 
may live forty, fifty, or sixty years. 

Diagnosis. — A cretin is usually recognizable at sight; but in some 
cases the phenomena are not marked (semicretins ; moderate hypo- 
thyroidism) and the condition may be overlooked. Achondroplasia 
(foetal rickets, fcetal chondrodystrophy), a peculiar form of dwarfism, 
may be distinguished by marked shortening of the extremities (micro- 
melia), great enlargement of the joints (hyperplasia of the cartilages), 
and absence of myxcedema, cretinoid expression, and defective mentality. 
Infantilism is characterized by an infantile condition of the genitalia 
and the absence of secondary sexual characteristics, but there is no 
myxcedema or other cretinoid characteristics. Idiocy, hydrocephalus, 
etc., should be readily distinguished. 

Prognosis. — The disease is progressive without specific treatment. 
Death often occurs early in life, but if the subject survives a few years, 
life may be prolonged forty or more years. 

Myxcedema of Adults.— Myxcedema of adults is a disorder occurring 
spontaneously in adults, due to a lack of thyroid secretion, and character- 
ized by myxcedema, physical weakness, and mental deterioration. The 
disorder is six to seven times as common in women as in men, and is 
most common in adult life (thirtieth to the fiftieth year). It may be 
hereditary or familial; or one member may have exophthalmic goitre 
and another myxcedema, etc. The thyroid is usually atrophic or absent ; 
if of normal size or enlarged, the epithelium is atrophic and degenerated. 
The thymus and the pituitary have been found enlarged. 

Symptoms.— The onset is usually insidious. The patient is believed 
to be " taking on flesh;" but the skin becomes harsh, dry, pale, inelastic, 



348 DISEASES OF THE THYROID GLAHD 

thickened, and apparently cedematous (but does not pit on pressure 
— myxcedema). Thick pads of such tissue may develop on the abdo- 
men, buttocks, thighs, supraclavicular regions, etc. The face becomes 
broad, swollen, and coarse, the lips, nose, and tongue thick, and the 
expression dull and listless; there is often a characteristic flush on the 
cheeks. The gait has been likened to that of a hippopotamus. Physical 
weakness progresses and may become extreme; and to this is joined 
mental apathy, slowness of thought and speech, defective memory, 
somnolence, and eventually dementia (which may be preceded by 
delirium, mania, etc.). The temperature is usually subnormal. There 
may be various paresthetic phenomena or actual neuromuscular pains 
(especially in the calves); undue sensitiveness to cold; arteriosclerosis 
with hypertrophy and dilatation of the heart; indigestion and constipa- 
tion; albuminuria or glycosuria; uterine and other hemorrhages; anemia, 
etc. 

Postoperative Myxoedema. — Cachexia strumipriva is a myxcedema- 
tous condition with the attendant physical and mental deterioration that 
develops after complete and sometimes after partial removal of the 
thyroid body. The amount of gland necessary to prevent this form 
of myxoedema has not been determined, but a small part, less than one 
lobe, usually suffices. The symptoms are quite the same as those 
of spontaneous myxcedema in the adult. 

Diagnosis. — Myxcedema should be recognized readily by attention to 
all the phenomena, cutaneous, physical, and mental. Obesity should be 
readily excluded. Bright's disease, suggested by the pallor and sub- 
cutaneous swelling, perhaps albumin and casts, should be readily excluded 
by the absence of pitting on pressure, and by the thickness, induration, 
and dryness of the skin, loss of hair, subnormal temperature, marked 
asthenia, and the mental phenomena. Incomplete or mild cases are 
likely to be overlooked, being mistaken for neurasthenia, psychasthenia, 
senile dementia, etc.; but careful investigation will disclose the asthenia, 
the mental apathy, the myxedematous condition of the skin, the small 
thyroid, etc. 

Prognosis. — The disease is steadily progressive in the absence of 
specific therapy. 

Treatment. — Deficiency of thyroid secretion, cretinism, and myxcedema 
are imperative indications for the use of thyroid preparations — a specific 
treatment. Usually the thyroid of sheep is used, beginning with one 
grain (0.06 gram) thrice daily and gradually increasing to fifteen grains 
(1 gram) or more a day or until the point of toleration (thyroidism) is 
reached (nervousness, cutaneous flushing, paresthesias, muscular twitch- 
ings or tremors, tachycardia, and other phenomena suggesting exoph- 
thalmic goitre). The effects are inconceivable to those unacquainted 
with them. After cure or marked improvement has been effected by 
large doses, smaller doses must be continued to insure permanency of 
results and prevent relapse. Good food, good hygiene, fresh air, hydro- 
therapy, and tonics (iron, arsenic, etc.) are useful adjuvants. 



DISEASES OF THE PARATHYROID GLANDS 349 



TUMORS AND CYSTS OP THE THYROID. 

Tumors of the thyroid may be benign (?) or malignant — adenoma, 
carcinoma, and sarcoma. An adenoma develops as a solid, encapsu- 
lated, usually soft, and smooth, growth in one lobe of the thyroid, 
compressing the normal thyroid tissue. It may be of the foetal type — 
solid, close vesicles, with little connective tissue stroma, and no colloid; 
or of the mixed type — solid vesicles without, and large, distended vesicles, 
with colloid; or of the papuliferous cystic type — cystic vesicles with 
papuliferous ingrowths. In addition to cystic formation (softening) these 
growths are prone to hemorrhage; and that they are not benign, or at 
least do not remain benign, is evident in the fact that they (especially 
the papilliferous cystadenoma) may give metastases; and that they pro- 
ceed by gradual histological variations to definite carcinoma. Sarcoma 
is rare, and may be of any of the common types. As a rule, tumors 
remain for a considerable time unsuspected, being not distinguished (and 
often indistinguishable) from simple goitre (hypertrophy); but malignant 
goitre should be diagnosticated in unilateral enlargements in adults, 
especially if the growth is rapid and nodular. The diagnosis, however, 
often is not made until the growth has penetrated the capsule, formed 
adhesions to adjacent tissue, and given rise to metastases to the regional 
lymph nodes or to distant parts, such as the lungs and the bones (a 
solitary bony metastasis — inferior maxilla, skull, sternum, etc. — being 
quite characteristic). In the differential diagnosis one must exclude 
the rare large solitary tubercle and a gumma. 

In addition to the softening and hemorrhagic cysts already mentioned, 
the thyroid may be the seat of echinococcus cyst. Aberrant or accessory 
thyroids are sometimes encountered at the base of the tongue, in the 
mediastinum, pleura, etc., and by proliferation may give rise to tumor 
formations. 



DISEASES OF THE PAKATHYROID GLANDS. 

Pathological Physiology. — The parathyroid glands (or bodies) consist, 
as a rule, of two pairs, upper and lower (four glands, sometimes six or 
eight), somewhat flattened and ovoid in shape, from 6 to 8 mm. long 
by 1 to 3 mm. in diameter, situated along the posterior inner edge of the 
lateral lobes of the thyroid. The physiological activities of the para- 
thyroids have not jet been completely worked out; but the glands seem 
to b>e essential to life and to be intimately concerned in the calcium meta I >- 
olism. Operative removal, as has been demonstrated in the lower animals, 
and in human subjects (unintentional removal or deprivation of blood 
supply when removing the thyroid), results in tetany— hypoparathyreos is 
or cachexia parastrumipriva (Halsted). The phenomena may be ameli- 
orated by feeding parathyroid preparations, and by injections of calcium 



350 , DISEASES OF THE PARATHYROID GLANDS 

salts; and they may be prevented by autotransplantation of the para- 
thyroids (Halsted). The parathyroids are doubtless in some unknown 
way related to the other ductless glands (through the medium of 
hormones) . They seem also to exercise some influence (antagonistic to 
that of the thyroid) on carbohydrate metabolism: following extirpation 
of the parathyroids, adrenalin glycosuria is readily produced, that is, the 
limit of carbohydrate metabolism is reduced. 

The parathyroids have been supposed also to be concerned in other 
convulsive disorders, such as epilepsy, myoclonia, myotonia, paralysis 
agitans, but upon insufficient evidence. Degeneration and sclerosis of 
the parathyroids have been found in infantile atrophy (R. L. Thompson). 
Tumors occasionally occur. Parathyroid preparations have been used 
with success in parathyroid insufficiency (tetany); and without success 
in Graves' disease, mvxcedema, convulsive disorders, etc. 



TETANY. 

Tetany is a disorder characterized by bilateral tonic, intermittent or 
continuous spasms of the extremities, and increased mechanical and 
electrical excitability of the peripheral nerves. 

Etiology. — Tetany sometimes occurs endemically or epidemically 
in certain parts of Europe (Berlin, Vienna, etc.), but it is rare in this 
country. In Europe it is especially common in young men of the 
artisan class, such as shoemakers, tailors, etc. It sometimes occurs 
in infections, such as typhoid fever, scarlatina, measles, cholera, etc. ; in 
intoxications, such as chloroform, lead, and ergotin poisoning, uremia, 
etc. ; in gastro-intestinal disorders, such as dilatation and other disorders 
of the stomach with retention; and in pregnancy and during lactation 
(nurse's contracture, Trousseau). It also follows operation upon and 
excision of the thyroid (removal or destruction of the parathyroids). 
In children it is usually associated with rickets, but sometimes also with 
acute infections, gastro-intestinal disorders, etc. 

The nature of the disorder is still somewhat imperfectly understood, 
but the researches of McCallum and Voegtlin and others suggest that it 
is due to insufficiency of the parathyroids and disturbance of the calcium 
metabolism. The parathyroids in some ill-understood way control 
the calcium exchanges in the body, and the absence or perversion of 
the parathyroid secretion leads to impoverishment of the tissues as 
regards calcium, perhaps by permitting calcium to combine with other 
substances and thus to be abstracted from the tissues. The result of this 
calcium impoverishment is hvperexcitability of the nerve cells and tetany; 
so that tetany may be regarded as a state of hvperexcitability of the nerve 
cells due to calcium impoverishment. 

Symptoms. — The chief symptom consists of bilateral, tonic, painful, 
intermittent, or continuous spasms of the muscles of the hands (accou- 
cher's hand), and less frequently of the feet (equinovarus position); 



DISEASES OF THE ADRENALS 351 

rarely the wrists, arms, face, legs, etc., may be involved. There is also 
increased mechanical excitability of the nerves: tapping the facial, 
median, ulnar, perineal nerves, etc., serves to provoke contracture 
(Chvostek's sign); and compression of the nerves provokes the same 
result (Trousseau's sign). The attacks continue for a variable time: 
in children often only an hour or two, in adults sometimes for a week or 
two — with exacerbations and remissions. There is also increased 
electrical excitability of the nerves: of the motor nerves to the galvanic 
current (Erb's sign), of the sensory nerves (Hoffmann's sign), and of the 
nerves of special sense (F. Chvostek's sign). The sensorium, as a rule, 
is not involved, and there are no objective sensory changes. In severe, 
acute cases there may be fever. Laryngismus stridulus sometimes 
occurs also in rickety children. 

Diagnosis. — The peculiar bilateral spasms and the increased mechan- 
ical and electrical excitability of the nerves are quite pathognomonic. 

Prognosis. — The prognosis varies with the associated conditions, being 
serious in operative tetany, in gastric tetany, and in laryngismus stridulus. 

Treatment. — The treatment varies with the etiological factors. In 
rickets, infections, and intoxications, the treatment is that of the under- 
lying cause. Weaning the child often cures the cases occurring during 
lactation. In the gastric cases lavage with saline and mild antiseptic 
solutions is sometimes efficacious. In operative tetany benefit accrues 
from the use of parathyroid preparations, and perhaps also from the 
subcutaneous transplantation of parathyroid bodies. The acute symp- 
toms are effectively controlled by the intravenous injection (less effec- 
tively by the subcutaneous injection or ingestion) of 5 per cent, solution 
of calcium lactate (or acetate), in physiological saline solution — 1000 
to 2000 c.c. at a time; magnesium salts also may be used. Chloral, 
bromides, and morphine may serve as useful adjuvants. 



DISEASES OF THE ADRENALS AND THE 
CHROMAFFIN SYSTEM. 

Pathological Physiology. — The adrenals, composed of readily differen- 
tiated cortex and medulla, are partly of epithelial and partly of nervous 
origin. The cortex in all probability is derived from the coelum epi- 
thelium; the medulla is derived from the sympathetic nervous system, 
and consists in large part of peculiar polymorphous cells, which in chromic 
acid solutions (chromic acid salts) take on a brownish pigmentation, 
and are, therefore, spoken of as chromaffin cells. Similar cells are found 
elsewhere in the sympathetic nervous system and its derivatives — the 
ganglia and larger nerve trunks of the sympathetic, as well as in certain 
so-called paraganglia, especially along the course of the aorta near its 
bifurcation (Zuckerkandl's bodies), the carotid glands, the coccygeal 
gland, collection of cells in the parovarium, in the epididymis, etc. — 



352 DISEASES OF THE ADRENALS 

all of which collectively are spoken of as the chromaffin system. Similar 
cells have been found also in aberrant adrenal rests and in the pituitary 
body. 

The functions of the adrenals are not completely known. The organ 
seems to be essential to life; removal in lower animals soon leads to death 
in the picture of severe intoxication. The cortex is believed to exercise 
a detoxifying function, neutralizing circulating poisons of intermediate 
metabolism; and to control, at least in part, growth and development, 
especially of the sexual organs (the adrenals of animals enlarge during 
sexual activity and pregnancy; cortical hyperplasia and tumor forma- 
tions are sometimes associated with precocious sexual development, 
and hypoplasia with retarded sexual development). The medulla 
and the chromaffin system throughout the body contain adrenalin, 
which may be looked upon as the specific product of the chromaffin 
system. Its chief function is the maintenance of blood pressure (through 
its stimulating action upon the vasoconstrictor fibers of the sympathetic) 
and of muscular tone, perhaps by furthering oxidation in the tissues. 
It probably exercises some influence on carbohydrate metabolism, since 
subcutaneous or intravenous injections give rise to glycosuria. The 
chief evidence of disordered function is cardiovascular and muscular 
asthenia (adrenal insufficiency), which is most marked in Addison's dis- 
ease. Less grades of such asthenia are common in many exhausting and 
debilitating diseases, and have been attributed to adrenal insufficiency. 
Some of these, such as pulmonary tuberculosis, gastric carcinoma, etc., 
may be associated with increased cutaneous pigmentation (as in Addison's 
disease), and others, such as neurasthenia, etc., with low blood pressure. 
In some infections (diphtheria) and other disorders, the myasthenia 
may come on suddenly and be very severe, and may be associated with 
lessened blood pressure; the condition may be relieved by adrenalin; 
in some fatal cases the adrenals have been found lacking in adrenalin, so 
that a condition of acute adrenal insufficiency has been postulated. 
Less severe cases are spoken of as subacute and chronic adrenal insuffi- 
ciency (incomplete Addison's disease). Whether an excess of adrenalin 
is ever formed is not known, but the well-known fact that adrenalin 
provokes arteriosclerosis in the lower animals has led to the supposition 
that it may be active in the causation of arteriosclerosis in man, and also 
to the suggestion that the metabolic products retained in the body in 
renal disease stimulate the adrenal medulla to increased functional 
activity, and that the increased adrenalin thus formed is the cause of 
the excessive blood pressure. Perhaps through some other influence 
an excess of adrenalin may be formed (or adrenalin may not be 
excreted), and lead not only to the heightened blood pressure, but 
also to the renal and cardiac changes of chronic cardiovascular-renal 
disease. 

Preparations of the adrenal (adrenalin) injected intravenously or sub- 
cutaneously are valuable in increasing the blood pressure in shock and 
conditions of low vascular tension generally (such as infections, intoxi- 



ADDISON'S DISEASE 353 

cations, etc.); and they are of service in controlling hemorrhages from 
surfaces to which they can be applied locally. 

Aside from Addison's disease and tumor formation, the adrenals are 
rarely the seat of disease of clinical interest. Degenerative changes 
(cloudy swelling, fatty and amyloid degeneration) accompany similar 
conditions in other organs. Hemorrhages occur in the newborn (espe- 
cially after difficult labors and still births), traumatisms, toxic and infective 
processes. They may give rise to pain in the upper abdomen, vomiting, 
collapse, convulsions, tympanites, diarrhoea, etc., and death. Tumors 
(hypernephromas) partake of the characteristics of retroperitoneal 
growths. Tumors of adrenal tissue also are common in the kidney 
(hypernephroma being the most common tumor of the kidney in the 
adult), and elsewhere along the genito-urinary (especially the female 
genital) tract. 

ADDISON'S DISEASE. 

Addison's disease is a disorder due to adrenal inadequacy (hypo- 
epinephry) characterized anatomically, as a rule, by tuberculosis of the 
adrenals and degenerative lesions in the chromaffin system elsewhere, 
and clinically by muscular and vascular asthenia, gastro-intestinal 
irritability, and pigmentation of the skin and mucous membranes. 

Etiology. — The disorder is most common in young adults (before the 
fortieth year), and is almost twice as common in males as in females. 
The etiological factors are those of tuberculosis and of tumor formation 
in general, and are as ill understood. 

Pathology. — Usually there is fibrocaseous tuberculosis of the adrenals 
— unilateral or bilateral; less commonly there is simple atrophy with 
associated fibrosis, or tumor formation. In addition, as Wiesel has 
pointed out, the chromaffin cells of the sympathetic nervous system 
(adrenal medulla, abdominal plexuses, etc.) disappear; the cortical 
substance of the adrenals may be preserved, as well as accessory 
adrenals, if any be found. Many of the ganglion cells exhibit not 
only the lipochrome pigmentation (which is not specific), but also 
the specific chromaffin reaction (characteristic of Addison's disease). 
Wiesel believes Addison's disease to be a specific affection of the chro- 
maffin system, consisting of successive atrophy of the chromaffin tissue, 
the process involving the adrenal medulla and spreading to the cortex; 
to compensate for this loss of chromaffin tissue some of the ganglion cells 
become chromaffin. The cases of extensive adrenal tuberculosis without 
clinical signs of Addison's disease are explained on the basis of absence 
of general disturbance of the chromaffin system; and the cases of Addi- 
son's disease without disease of the adrenal are believed to be due 
probably to the fact that lesions of the chromaffin system outside the 
adrenal are sufficient to produce the symptom-complex of the disease. 

Symptoms. — The following is adapted from Addison's classical 
description: The patient is observed gradually to fall off in general 
23 



354 DISEASES OF THE ADRENALS 

health; he becomes languid and weak, indisposed to bodily or mental 
exertion; the appetite becomes impaired or entirely lost; the whites of the 
eyes become pearly, the pulse small and feeble, or perhaps somewhat 
large, but excessively soft and comprehensible; the body wastes, without, 
however, presenting the dry and shrivelled skin and extreme emaciation 
usually attendant on protracted malignant disease; slight pain or uneasi- 
ness is, from time to time, referred to the region of the stomach, and 
there is occasionally actual vomiting which may be both urgent and dis- 
tressing; and the patient may manifest indications of disturbed cerebral 
circulation. Gradually a characteristic discoloration of the- skin becomes 
apparent; this pervades the whole surface of the body, but is commonly 
most marked on the face, neck, arms, penis, and scrotum, and in the 
flexures of the axillae and around the navel ; it presents a dingy or smoky 
appearance or various tints of deep amber or chestnut-brown; it may 
occur in patches, or certain parts may be so much darker than others as 
to impart to the surface a mottled appearance; and in the midst of this 
dark mottling certain insular portions of the skin may present a blanched 
or morbidly white appearance (actual defect of pigment), contrasting 
strongly with the surrounding skin. Similar irregular distribution of 
pigmentation may occur in the mucous and serous membranes. This 
singular discoloration usually increases with the advance of the disease; 
the anemia, languor, failure of appetite, and feebleness of the heart 
become aggravated; the body wastes; the pulse becomes smaller and 
weaker; and without any special complaint of pain or uneasiness the 
patient gradually sinks and expires. 

Diagnosis. — Muscular, vascular, and mental asthenia, pigmentation of 
the skin and \isible mucous membranes, and gastro-intestinal symptoms 
(pain, vomiting, and diarrhoea) are quite diagnostic, especially when, 
as stated by Addison, " neither the most diligent inquiry nor the most 
careful physical examination tend to throw the slightest gleam of light 
upon the precise nature of the patient's malady." The maximum blood 
pressure may be 100 mm. Hg. or less. The blood shows the ordinary 
changes of secondary anemia (which excludes pernicious anemia). Other 
sorts of pigmentation must be excluded, such as that of dark-skinned 
races; pregnancy and disease of the female genitalia; vagabond's disease 
(pigmentation of exposed parts; rough and scratch-marked skin; often 
associated pediculi); pernicious anemia; Graves' disease; diseases of 
the stomach, especially carcinoma; chronic jaundice; hemochromatosis 
(bronzed diabetes); chronic malaria; pellagra; melanosarcoma of 
the skin; chronic poisoning with silver nitrate (argyria), arsenic, etc. 
It is wise to withhold the diagnosis in the absence of asthenia. In case 
of doubt resort may be had to tuberculin tests, but positive results must 
be interpreted cautiously, since they may be due to tuberculosis else- 
where than in the adrenals. 

Prognosis. — The disease is doubtless invariably falal. The common 
duration is about three or four years from the onset of symptoms, but 
this may be influenced by tuberculosis elsewhere in the body. Some- 



DISEASES OF THE PITUITARY BODY 355 

times remissions or standstill ensue and the patient may live ten or 
more years. Rarely there are what are called acute cases (acute adrenal 
inadequacy), in which, with marked asthenia, vomiting, diarrhoea, and 
the general evidences of severe intoxication, death may ensue w r ithin a 
few weeks. 

Treatment. — The treatment is almost wholly symptomatic: rest in bed 
on account of the asthenia and a tendency to marked and perhaps fatal 
syncope; good nutritious diet — especially milk; strychnine and arsenic 
as general tonics; bismuth, creosote, carbolic acid, cerium oxalate, dilute 
hydrocyanic acid, etc., for the gastro-intestinal irritability. The use of 
adrenal preparations by the mouth, subcutaneously, and intravenously, 
is indicated theoretically; practically their use has been attended by 
diverse results : they seem to be of much value early, in doses to suit the 
exigencies of individual cases. Tf a tumor or salivary tubercle of the 
adrenal can be diagnosticated it should be removed. 



DISEASES OF THE PITUITARY BODY. 

Pathological Physiology. — The pituitary body, or hypophysis cerebri, 
is composed of two lobes — an anterior, the larger, of epithelial origin 
(a diverticulum of the buccal epithelium), and a posterior, smaller, 
in part of nervous origin (infundibular pouch of the thai amen cephalon) 
and in part of epithelial origin, the two being separated by a persisting 
cleft. The physiological properties of the pituitary body have not 
been definitely determined, although the body seems to be essential 
to the maintenance of life. The posterior lobe (doubtless the nervous 
nucleus) contains a blood-pressure-raising substance (pituitarin) and 
a diuresis-producing substance (increasing the blood pressure or 
acting directly on the renal epithelium). The anterior (perhaps more 
important) lobe is believed to exercise some influence over bodily growth 
and sexual development. Augmented function (hyperpituitarism), such 
as may occur in hypertrophy and tumor formations, and is perhaps 
referable to increase in number or overactivity of the chromophile cells 
(less likely subactivity of the chromophobe cells), seems to lead to gigant- 
ism if it occurs during early life, and to akromegaly if it occurs during 
adult life. Deficient function (hypopituitarism) occurring in early life 
seems to lead to certain types of infantilism associated with excessive 
deposition of fat and imperfect development of the sexual organs and of 
the secondary sexual characteristics; perhaps the loss or retrogression of 
these sexual characteristics in adult life may be due also to hypo-activity 
of the pituitary. Removal of the gland in lower animals has led to the 
development of a condition comparable to that believed to be due to 
hypopituitarism in man; and excision of the enlarged body in akro- 
megaly had been followed by notable improvement (Gushing). The 
pituitary also bears some relationship to the other ductless glands: it 
has been found enlarged after excision or disease of the thyroid and 



356 DISEASES OF THE PITUITARY BODY 

adrenal, and it (especially the posterior lobe) is said to contain a sub- 
stance (hormone) that stimulates the adrenal and inhibits thyroid activity, 
while the anterior lobe is said to stimulate thyroid activity. 



AKROMEGALY. 

Akromegaly is a disease, probably due to disordered function of the 
pituitary body, and characterized by abnormal growth especially of the 
face, hands, and feet. 

Etiology. — Akromegaly is about equally common in the two sexes, 
and is most common in the third decade (75 per cent, of the cases); it 
is rare before the twentieth and after the fortieth year. There is no 
known cause, ascribed factors, such as shock, fright, alcoholism, syphilis, 
etc., being of more than doubtful significance. 

Pathology. — The majority of cases exhibit some more or less obvious 
disease of the pituitary, notably tumor formation (adenoma, carcinoma, 
sarcoma), but sometimes softening, hemorrhage, and fibrosis; microscopic 
lesions have been found in some pituitary bodies normal to the unaided 
eye. The bones of the skull, and those of the hands and feet, especially, 
but also the other bones of the body to a greater or less extent, become 
enlarged, thickened, and denser than normally. The enlargement is 
due to periosteal overgrowth, and involves particularly the bony promi- 
nences. The soft tissues of the extremities also become thickened — by 
connective tissue hyperplasia and fibrosis (answerable for much of the 
enlargement). The other ductless gland sometimes shows divers, but 
no constant, changes. The viscera (heart, liver, spleen, kidneys, etc.) 
are sometimes enlarged. The pancreas may be fibrosed. The internal 
genitalia may be enlarged, but the testicles, uterus, and ovaries, usually 
are atrophic or degenerated. 

Symptoms. — The bony enlargements are sometimes the earliest symp- 
toms, but in the majority of cases antecedent symptoms referable to the 
overgrowth of the pituitary (brain tumor) may be elicited: headache, 
vertigo, vomiting, mental irritability and other alterations, disturbance 
of the special senses (sight, hearing, and taste), and of the cranial nerves 
(optic neuritis, oculomotor and other paralyses). These, if not developed 
early, are likely to supervene later. In addition there may be pares- 
thesias, more or less severe pains, etc., in the extremities. The charac- 
teristic of the disease is abnormal growth, especially of the face, hands, 
and feet — which, although much enlarged, are not, as a rule, otherwise 
deformed. The head increases in size, but less so than the face, which 
in consequence of marked growth of the superior and (especially) the 
inferior maxilla, becomes elongated. The teeth become separated, from 
widening of the alveolar arches. The hands and feet show one of two 
types — the long or the thick (spade-like, sausage-like fingers). The 
hypertrophy involves also the soft parts of the hands and feet, and face 
(nostrils, lips, eyelids, cheeks, ear, tongue, etc.). Later, other bones (ster- 



AKROMEGALY 357 

num. ribs, vertebrae, etc.) may become involved, and kyphosis, etc., may 
supervene. The skin, in general, may become harsh, dry, and thickened 
(perhaps remotely suggesting myxcedema), or there may be profuse 
sweats; sometimes also the mucous membrane of the mouth, nose, larynx, 
etc., becomes thickened. The muscles may become atrophic, the huge 
frame and bulk of the subject then contrasting markedly with the general 
muscular weakness. Sexual disorders are common — amenorrhoea in 
women, impotence in men. Glycosuria sometimes supervenes. Arterio- 
sclerosis and hypertrophy and dilatation of the heart are common. 
The viscera (liver, spleen, and kidneys) may become enlarged, and 
the lymph nodes and the thymus may become palpable. 

Diagnosis. — The disease is usually recognized on sight. Especial 
attention should be paid to bitemporal hemianopsia, optic neuritis or 
atrophy, oculomotor paralyses, and other symptoms of tumor in the 
sella turcica, as early signs. Gigantism, osteitis deformans, and hyper- 
trophic pulmonary osteo-arthropathy must be differentiated. 

Prognosis. — The disorder is progressive, but often lasts for many 
(twenty or more) years. Death results from general asthenia, secondary 
infection, brain tumor, cardiac weakness, diabetes, etc. 

Treatment. — There is no known efficacious medical treatment. Oper- 
ative removal of at least a part of the enlarged pituitary appears to be 
the treatment of the future; it has already been successfully done with 
benefit by Cushing. 



SECTION V. 

DISEASES OF THE BLOOD AND HEMOPOIETIC 

SYSTEM. 



Pathological Physiology. — The blood is a tissue as well as a fluid — a 
tissue reflecting the state and condition of the so-called hemopoietic 
organs, of which it is the circulating portion; and a fluid containing the 
soluble products of the metabolic activities of all the component parts of 
the body. Morphologically it is of comparatively simple constitution, con- 
sisting of erythrocytes, leukocytes, platelets, and plasma; but chemically 
it is of exceedingly complex composition. It subserves primarily the func- 
tion of conveying to the body-cells oxygen and absorbed food products, 
essential to their life and well being, and of receiving and disposing of the 
products of cellular activity, whether these be refuse or of further use in 
the economy; but, in addition, the blood is charged with another most 
important function — that of defense against divers infectious and toxic 
processes to which the body is constantly exposed. Thus, it represents 
the sum total of the activity and inactivity, the anabolism and katabolism, 
and normal and perverted function of all the tissues and organs of the 
body, of which it is the connecting link. 

So subject is the composition of the blood to the influences of extra- 
circulatory conditions that disorders of the blood must be largely, if not 
wholly, merely a reflection of diseased processes elsewhere. Is the body 
anywhere diseased, so also is the blood; divers toxic processes, such as 
accompany infections, intoxications, and disorders of metabolism, like 
diabetes, gout, uremia, etc., are in a sense disorders of the blood: so 
that one may well doubt whether the blood is ever primarily diseased. 
In a general sense also one may say that the hemopoietic system com- 
prises all the tissues and organs of the body, since each contributes its 
moiety to the composition of the whole. But since custom and con- 
venience sanction a separate discussion of disorders in which changes 
in the blood are noteworthy, so also they sanction restriction of the 
term hemopoietic organs to those concerned in the production of the 
formed elements of the blood. 

In the foetus this hemopoietic system consists of the bone marrow, the 
lymph nodes, the spleen, and the liver, and there is no sharp line of 



360 DISEASES OF THE HEMOPOIETIC SYSTEM 

differentiation between the tissues producing erythrocytes, on the one 
hand, and leukocytes, on the other. At birth the liver has lost its blood- 
forming function; and as growth continues the other hemopoietic organs 
gradually become specialized, so that in adult life the erythroblastic 
and the leukoblastic tissues are sharply differentiated, although under 
the stress of circumstance they may revert to the foetal type. In adult 
life the erythrocytes are formed in the red marrow of the bones by divi- 
sion or loss of the nuclei of the erythroblasts, which in turn, perhaps, are 
derived from colorless, mononuclear, non-granular mother cells that 
take on hemoglobin; it is believed that in some diseased states the hemo- 
lymph nodes also may form erythrocytes. The granular leukocytes are 
formed in the bone marrow, being derived from certain mononuclear 
neutrophilic, eosinophilic, or basophilic cells, which in the course of time, 
and usually before they enter the circulation, develop polymorphous 
nuclei, and give rise to the polynuclear neutrophiles, eosinophiles, and 
basophiles (so-called mast-cells) of the circulating blood. The origin 
of the so-called mononuclear leukocytes is still in dispute, although the 
weight of evidence assigns them to the bone marrow; perhaps they are 
mother cells. The lymphocytes are formed in the lymph nodes, thymus, 
tonsils, and lymphoid tissues generally throughout the body. In the 
central portions of the so-called germ centres, where proliferation is active, 
the cells are large and correspond with the large lymphocytes of the cir- 
culating blood, but toward the periphery of the germ centres, the cells 
are smaller and correspond with the ordinary small lymphocytes of the 
circulating blood. Whether any circulating lymphocytes are formed in 
the bone marrow in health is not definitely known, although it seems 
likely; but in diseased states, such as leukemia, the marrow contributes 
large numbers of so-called lymphocytes — probably not identical with the 
circulating lymphocytes of health. There is considerable evidence that 
both the red and the white cells are derived from a common ancestor — a 
large mononuclear, non-granular, somewhat basophilic marrow cell; 
but when once started on their life journey, cells of the one series cannot 
become converted into the other. The blood platelets, according to 
the studies of J. H. Wright, are formed by detachment of the pseudo- 
pod-like processes of the giant cells (megakaryocytes) of the bone marrow. 
The erythrocytes are designed to absorb and diffuse oxygen and per- 
,haps carbon dioxide — their sole known function — which they effect by 
reason of their contained hemoglobin, and for which their flexibility 
and biconcave surface admirably adapts them. The functions of the 
leukocytes are ill understood: endowed with independent motility, 
they appear to be concerned in the absorption of fat and protein from 
the intestine and in other nutritive (cellular) processes; they contribute 
to the clotting of blood by producing fibrin ferment, thrombokinase; they 
produce also apparently a fat-splitting and a tryptic ferment; they 
facilitate the repair of injuries; they are especially concerned in various 
defensive processes (phagocytosis) whereby the body is enabled to resist 
bacterial invasion; and they act as scavengers in removing animate and 



ANEMIA 351 

inanimate foreign substances that act as sources of irritation. But their 
function is doubtless more comprehensive. The polynuclear leukocytes 
are those especially concerned in phagocytosis; the eosinophils, while 
non-phagocytic are especially concerned in parasitic infections; the 
mast-cells and the lymphocytes also doubtless have specific functions, 
although they are unknown. The blood platelets are much concerned in 
coagulation of the blood (whence they have been termed thrombocytes) ; 
they are diminished in conditions, such as pernicious anemia, purpura, 
typhoid fever, etc., in which clotting is poor and the bone marrow 
deficient in megakaryocytes. 

The blood doubtless varies considerably in composition from time to 
time under various influences, but the remarkable fact is its tendency 
to maintain a uniform composition under many and varied conditions. 
Normally the erythrocytes number about 5,000,000 to the cubic milli- 
meter in man, and 4,500,000 in women; the leukocytes, 6000 to 10,000 
(averaging about 7500); and the platelets, 200,000 to 700,000. The 
plasma also tends to maintain a uniform composition by the excretion 
of deleterious substances through the kidney, skin, and lungs, and, as 
occasion demands, absorbing from or discharging into the lymph 
channels some of its substance. 

The circulating blood corpuscles are believed to enjoy only a brief life 
career. The erythrocytes are credited with an average life of three or 
four weeks, but this is not susceptible of proof. They probably gradu- 
ally succumb to the stress of a strenuous existence, and are finally com- 
pletely destroyed in the spleen and liver, perhaps even in the vascular 
channels, and at least in certain diseased states in the hemolymph 
nodes. The life span of the leukocytes is not known; they are believed 
to succumb even earlier in circulatory life than the erythrocytes, and 
to find their campo santo in the spleen. 

Anemia. — What otherwise would be an early dearth of blood corpuscles 
is prevented by continued new formation. This, which suffices in health 
to maintain a uniform standard, may prove insufficient in disease, or it 
may fail entirely. The ensuing, corpuscular deficiency is spoken of as 
anemia, a term that properly comprises a lessening of the total volume 
of the blood or a deficiency of any one of its constituent elements, 
corpuscles, hemoglobin, or albuminous and other constituents of the 
plasma. Changes in the plasma, however, are ill understood, and while 
in some cases they probably are of prime importance, clinically our 
attention is practically always directed to the corpuscles and the 
hemoglobin. 

Anemias are commonly divided into the primary and the secondary 
anemias. Strictly speaking all anemias are secondary, that is, the con- 
sequence of some underlying, though often overlooked, or unknown, 
cause. Since, however, the cause of some anemias cannot be ascer- 
tained, we may continue provisionally the designation primary, essential, 
or idiopathic anemia. These comprise chlorosis and pernicious anemia. 
Splenic anemia, leukemia, and Hodgkin's disease, sometimes here 



362 DISEASES OF THE HEMOPOIETIC SYSTEM 

included, are not in any sense primary anemias. Secondary or symp- 
tomatic anemias, those due to obvious causes, are further divided, 
according to their course, into acute and chronic. 

Anemia may be brought about by: (1) Hemorrhage; (2) lessened 
corpuscular production (deficient hemogenesis) ; or (3) increased destruc- 
tion (increased hemolysis); that is, by the loss of a considerable volume 
of blood or by causes that injure either the hemopoietic tissues or 
the corpuscles after they have been formed. Although deficient hemo- 
genesis is perhaps at the basis of chlorosis, the majority of cases of 
anemia result from increased hemolysis, to which, in cases of long-con- 
tinued or very severe anemia, defective and deficient hemogenesis may 
be added. The hemolysis may be induced by: (1) Bacterial toxins; (2) 
chemical poisons; (3) cellular and other hemolysins; (4) the action of 
heat (burns) and of cold (paroxysmal hemoglobinemia) — which either 
kill the erythrocytes outright or injure the enveloping elastic membrane 
and permit the diffusion of the contained hemoglobin into the plasma 
(hemoglobinemia). Similar results may ensue from changes in the pro- 
tein composition of the plasma, and from changes in the molecular con- 
centration (electrolytic conductivity by means of ions) of the plasma 
and consequent changes in osmotic tension. A plasma too rich or too poor 
in salts (ions) leads to shrinkage or swelling of the erythrocytes and loss 
of hemoglobin. The hemoglobin set free in the plasma is, as a rule, 
speedily removed by the spleen and liver, but in some cases (occasionally 
in malaria, paroxysmal hemoglobinemia, etc.), the hemolysis occurs so 
rapidly and to such an excessive degree that the liver, spleen, bone 
marrow, etc., are unable successfully to cope with it and hemoglobinuria 
results. The hemoglobin may become converted into methemoglobin, 
either in the cells or in the plasma. The consequences of anemia are 
obvious — reduction in the oxygen-carrying capacity of the blood and 
insufficient nutritive supply to the organs, particularly the brain and 
the heart. The factors inducing the anemia may or may not implicate 
the leukoblastic tissues, so that the white corpuscles may remain normal, 
or they may become increased (leukocytosis), or diminished (leukopenia). 

Following anemia — whatever its cause — regeneration of the corpuscles 
usually begins immediately, and it proceeds, sometimes slowly, some- 
times remarkably rapidly — the rate depending apparently upon the 
nature of the stimulus and the vitality of the erythroblastic and leuko- 
blastic tissues. Whatever the nature of the stimulus (infectious, toxic, 
chemotactic), it results at first in the discharge into the circulation of the 
already formed and warehoused mature cells — normal erythrocytes, 
polynuclear leukocytes, etc. Should these not suffice to restore and 
maintain the normal balance, more or less immature cells appear in the 
circulation — erythrocytes variable but rather small in size, distorted in 
shape, poor in hemoglobin, some, perhaps, nucleated and exhibiting 
polychromatophilia (evidence likely of immaturity rather than senility), 
and leukocytic antecedents of the polynuclear neutrophiles. The appear- 
ance of such cells in the circulating blood, then, is to be interpreted as an 



PLETHORA AND POLYCYTHEMIA 363 

effort on the part of the bone marrow to supply a deficiency. Under these 
circumstances the erythroblastic (red) centers in the bone marrow have 
become hyperplastic, have encroached upon and replaced more or less of 
the fatty (yellow) marrow of the long bones. In the more severe types 
of anemia, represented by the several varieties of pernicious anemia, in 
addition, to the foregoing, megalocytes and megaloblasts appear in the 
circulation in considerable number, and the bone marrow reverts to the 
foetal or juvenile type (megaloblastic degeneration, Ehrlich); that is, 
although red, as in milder anemias, it contains many large cells — meg- 
alocytes and megaloblasts. This is interpreted as evidence of overstrain 
and consequent inefficient effort to replace lost cells — the production of 
cells of the fcetal life (metaplasia of the erythroblastic tissue). In some 
cases the bone marrow ultimately becomes incapable of supplying the 
demand; it may become exhausted, or its activity may be inhibited by 
the initiating infectious, toxic, or other cause, and complete cessation of 
its function may ensue (aplastic anemia) : the bone marrow becomes pale, 
yellowish, or fatty throughout. In some cases the stimulus to activitv 
involves the leukoblastic rather than the erythroblastic tissues, and 
leukocytosis, leukemia, etc., result. In other cases inhibition of leuko- 
blastic activity and leukopenia ensue, as in some anemias, typhoid fever, 
cachexias, intoxications, etc. In leukemia and occasionally in other 
conditions (infections), the entire hemopoietic system (bone marrow, 
spleen, lymph nodes, even the liver) may revert to the fcetal type, and 
cells indistinguishable from bone-marrow cells may be formed in the 
spleen, lymph nodes, etc. Many of these cells partake of the undif- 
ferentiated, perhaps ancestral type. In lymphatic leukemia the normal 
granular series of bone-marrow cells may entirely disappear. In some 
cases the stimulus to activity is not specific, at least, not in its entirety, 
and both the erythroblastic and the leukoblastic tissues may be 
involved, as is exemplified in the occurrence of cells of the leuko- 
blastic series in some cases of severe anemia (ordinary pernicious 
anemia, leukanemia), and the marked reduction, if not total absence, 
of the leukocytic (granular, bone-marrow) cells in cases of aplastic 
anemia, etc. 

Plethora and Polycythemia. — An increase in the total volume of blood 
(so-called plethora) was formerly much believed in, but its existence is, 
at least, doubtful. One may suspect such a condition in a person, usually 
a man, who eats too much and drinks too much (especially alcohol), who 
is large in muscle and round in fat, who exhibits general cutaneous 
hyperemia and dilated venules of the face, and whose heart perhaps is 
large and arteries full and bounding. A serous plethora has been found 
to be common in chlorosis. More commonly there is an increased 
number of erythrocytes in a measured amount of blood (polycythemia I : 
physiologically in the newborn, and at high altitudes in consequence of 
lowered atmospheric pressure and consequent increased peripheral dis- 
tribution; and pathologically, in congenital heart disease, in acquired 
heart and pulmonary disease attended with blood stasis, in erythremia 



364 DISEASES OF THE HEMOPOIETIC SYSTEM 

with splenomegaly, and in cholera and other diseases in which the blood 
may become inspissated. 

Leukocytosis. — At birth the number of leukocytes varies from about 
14,000 to 19,000 per cubic millimeter; gradually the number diminishes, 
so that in adult life they average about 7500, the normal limit being 
usually set down as from 6000 to 10,000. They vary somewhat in the 
same individual from time to time. Under divers circumstances the num- 
ber may be increased beyond the normal limits, a condition spoken of as 
leukocytosis — which usually is temporary, but may last for some con- 
siderable time (subacute or chronic leukocytosis). In the short-duration 
cases the increased number of leukocytes is derived mainly from already 
formed cells resting or awaiting a summons in the sinuses of the bone 
marrow and the capillaries of the liver and lung; but in the long-duration 
cases new formation occurs and the bone marrow exhibits leukoblastic 
changes. Leukocytosis may be physiological or pathological. 

Physiological Leukocytosis. — An increased number of leukocytes is 
normal — at and for some time after birth; during the latter part of 
pregnancy and parturition; after a cold bath, exercise, and massage; 
and during digestion, particularly of a meal rich in protein. It is doubt- 
ful whether under any of these circumstances any new formation occurs ; 
probably there is only a redistribution of leukocytes already formed. 
The increase is scarcely if ever more than one-third of the normal, and 
the relative proportion of the different varieties of leukocytes remains 
unchanged. 

Pathological leukocytosis may be due to: (1) Infections, especially 
those associated with an inflammatory, purulent exudation. In these 
cases it is attributed to chemotactic influences, and there is probably a 
new formation of leukocytes. The absence of leukocytosis in some infec- 
tions is notable — typhoid fever, malaria, measles, rotheln, influenza, 
mumps, early stages of tuberculosis (except meningeal form), and leprosy. 
(2) Zooparasite invasions, especially trichinosis, uncinariasis, filariasis, 
echinococcosis, etc. (3) Intoxications, such as illuminating gas pois- 
oning, uremia, etc. (4) The cachexias of malignant disease and other 
marantic states. (5) Hemorrhage. (6) Terminal or preagonal states. (7) 
Certain drugs. The number of leukocytes usually varies between 15,000 
and 30,000; occasionally it may reach upward of 50,000, and very rarely 
even upward of 100,000. Although usually there is an increase of all forms 
of leukocytes, there is, in contrast to physiological leukocytosis, usually 
also a disproportionate or so-called relative increase in some one of the 
types, so that one speaks of polynuclear leukocytosis, large mononuclear 
leukocytosis, lymphocytosis (lymphemia), eosinophilia, basophilia, and 
myelocytosis (myelemia). Myelocytosis aside from myeloid leukemia is 
a rare occurrence; but a small percentage of myelocytes is occasionally 
seen in certain infections and more or less severe anemias, especially in 
children. Basophilia also is a rare and ill-understood condition; it occurs 
in myeloid leukemia and rarely in certain parasitic infections. Eosino- 
philia (5 to 30 per* cent, of the total number of leukocytes) is a significant 



ACUTE SECONDARY ANEMIA 365 

diagnostic sign of parasitic infections (trichinosis, uncinariasis, filariasis, 
ecchinococcosis, bilharziosis, etc.); it occurs also in certain skin disorders 
(urticaria, pemphigus, psoriasis, pellagra, purpura, etc.), in bronchial 
asthma, in myelocytic leukemia, in certain inflammatory exudates, etc. 
Lymphocytosis (a relative and absolute increase in the number of circu- 
lating lymphocytes) is normal in the infant; it is especially conspicuous 
in pertussis, and sometimes occurs in syphilis and certain forms of 
septicopyemia attended with lymph-node involvement; and it is the 
characteristic feature of lymphocytic leukemia. A large mononuclear 
leukocytosis (relative) sometimes occurs in malaria. The polynuclear 
neutrophilic leukocytosis is the most common and most important form; 
it occurs especially in infectious inflammations with or without suppura- 
tion. Significance attaches not only to an increase in the total number of 
leukocytes, but also to a relative increase (80 to 95 per cent.) of the poly- 
nuclear neutrophils, even when the total number of leukocytes is only 
slightly above the normal. The following opinions seem warranted: 
(1) An early and marked polynuclear leukocytosis is usually significant 
of good resistance to a more or less severe infection; (2) persistence or 
increase in the leukocytosis is significant of continued good resistance; 
(3) a slight total leukocytosis, or a relative polynuclear neutrophilic 
leukocytosis, may mean only a minor infection, or a severe, perhaps 
fulminating infection, against which the forces of resistance are more or 
less incapable of contending; (4) a delayed and then, perhaps, only 
moderate leukocytosis usually means a more or less severe infection 
and deficient resistance; (5) a high leukocytosis with increasing toxic 
manifestations, while signifying good resistance, does not preclude the 
possibility of ultimate exhaustion of all the body forces, including the 
powers of resistance as represented in part by the leukocytosis; (6) a 
moderate or high relative (as well as absolute) polynuclear leukocytosis, 
while often significant of suppuration, is more properly indicative of 
severity of infection which may or may not lead to suppurative exudation, 
depending upon the associated phenomena; the diagnosis of suppuration 
should be made upon all the clinical evidence, and not upon one sign 
(the leukocytosis) alone. 



ACUTE SECONDARY ANEMIA. 

Etiology. — Acute secondary anemia is almost always due to hemor- 
rhage, either external or internal, spontaneous or traumatic; in degree 
it usually corresponds with the rapidity and the total volume of blood 
lost. In rare cases acute anemia results from bacterial infection or 
intoxication, though these usually lead to subacute or chronic anemia, 
Infectious diseases, such as typhus, malaria, and typhoid fevers, and 
certain forms of sepsis, especially puerperal sepsis, and poisoning by 
nitrobenzol and other substances that rapidly destroy the blood (hemo- 
lysis), sometimes result in very acute anemia. 



366 DISEASES OF THE HEMOPOIETIC SYSTEM 

Pathology. — After death from very severe hemorrhages one usually 
finds fatty degeneration of the viscera, especially the heart muscle, the 
liver, the kidneys, and the stomach, and sometimes hyperplasia of the 
erythroblastic tissue of the bone marrow. 

Symptoms. — The symptoms of acute anemia consist of pallor of the 
skin and visible mucous membranes; increased frequency of the heart 
beat, anemic murmurs, and smallness and emptiness of the pulse; cool- 
ness of the extremities, and generally low body temperature; marked 
dyspnoea in consequence of the marked diminution in the oxygen- 
carrying constituent of the blood; thirst; evidences of cerebral anemia, 
such as faintness, spots before the eyes, noises in the ears, vertigo, nausea, 
vomiting, fibrillary tremors, and perhaps convulsions (in extreme cases). 
The amount of blood lost in some cases is extreme (rupture of an aneu- 
rysm, ectopic pregnancy, etc.), and may lead immediately to death 
from acute asphyxia and anemia of the brain ; but many patients survive 
very great and sudden losses — perhaps one-half of the total volume of 
blood. If not sudden, the loss of blood may be even greater, and the 
patient survive — repeated hematemesis, hemorrhages from duodenal or 
typhoid ulceration, etc. 

Examination of the blood reveals oligocythemia, and usually a dis- 
proportionate oligochromemia, so that the color index is usually low — 0.8 
or lower. The oligocythemia rarely reaches the high grade observed in 
pernicious anemia; thus, after repeated hemorrhages from gastric ulcer, 
the count may be scarcely less than 2,000,000 or 1,800,000. Regenera- 
tion of the blood begins almost immediately, and continues apace, so 
that in some cases of severe hemorrhage restitution is almost complete 
at the end of ten to fourteen days; usually, however, the normal condi- 
tion is not reached for several weeks or months. The hemoglobin value 
is restored less rapidly than the corpuscles, and may remain relatively 
low (low color index) for a considerable time. The total volume of the 
blood is usually soon restored by absorption of fluids (as well as salts) 
from the lymphatics and elsewhere. 

Microscopically, anisocytosis may be observed, and while a few ery- 
throcytes may be undersized, the majority appear swollen after severe 
hemorrhages; poikilocytosis is usually slight; polychromatophilia is 
often present early, but soon disappears; nucleated corpuscles (mostly 
normoblasts) appear early, sometimes in large numbers and inter- 
mittently, and may be found until restitution of the blood is complete. 
Significant of regeneration, the absence of erythroblasts augurs ill. 
The leukocytes are often slightly increased — polynuclear neutrophilic 
leukocytosis, which usually disappears with convalescence. Rarely 
slight lymphocytosis or myelocytosis has been observed. In severe cases 
the blood approaches that of pernicious anemia — marked oligocythemia, 
high color index, marked poikilocytosis, megalocytes, etc. 

Prognosis. — The prognosis varies with the amount of blood lost, the 
rapidity of the loss, the general condition of the patient at the time of the 
hemorrhage, and the evidences of regeneration. 



CHRONIC SECONDARY ANEMIA 367 

Treatment. — The treatment should consist of rest in bed, with depres- 
sion of the head; ligation of the bleeding vessel, if possible; and the injec- 
tion into the veins of a volume of physiological saline solution sufficient 
to maintain the circulation (500 to 2000 c.c.). Sterile 0.9 per cent, 
sodium chloride solution is commonly used, but a preferable solution 
(which must be sterilized) is the following: 

3$ — Sodium chloride 9|0 

Potassium chloride 1 

Calcium chloride 25 

Water 1000 

— Hare. 

In sudden severe hemorrhages likely to prove immediately fatal, Crile 
advises resort to rapid rhythmic pressure upon the chest with a view to 
produce artificial respiration and a moderate artificial circulation; at 
the same time, by means of a cannula inserted in a large artery near the 
heart, he injects some physiological saline (or Ringer's or Locke's) solu- 
tion, and as soon as the fluid has begun to flow, by means of a hypo- 
dermic needle inserted into the rubber tubing near the cannula, he 
injects 15 to 30 minims (1 to 2 c.c.) of adrenalin chloride, 1 to 1000; the 
injection may be repeated in a minute, if required. This brings about 
a rising arterial and coronary pressure, and stimulates the heart to 
renewed activity. Crile believes this treatment more effective than the 
use of stimulants, nitroglycerin, intravenous infusions, electricity, need- 
ling of the heart, or direct cardiac massage. The later treatment is that 
of the primary disease; and in addition, measures, to be mentioned under 
chronic anemia, designed to restore the blood to the normal. 



CHRONIC SECONDARY ANEMIA. 

Etiology. — Chronic secondary anemia may be due to: (1) Bacterial 
infections, whence it is a concomitant of all infectious diseases, especially 
typhoid fever, acute rheumatic fever, septicemia, diphtheria, syphilis, 
tuberculosis, etc. The anemia of the acute infectious diseases, however, 
is often subacute rather than chronic, and, as a rule, responds promptly 
to treatment. (2) Zooparasite infections, such as malaria and the 
different worms (Uncinaria americana, Dibothriocephalus latus, Filaria 
bancrofti, Schistosoma haematobium or japonicum), which often pro- 
duce an anemia scarcely distinguishable clinically from progressive 
pernicious anemia. (3) Intoxications, (a) biological (not separable from 
the infectious diseases); (6) inorganic, such as lead, arsenic, mercury, 
phosphorus, potassium, certain coal tar derivatives, etc.; (c) autogenic 
poisons, such as occur in disorders of the gastro-intestinal tract, 
nephritis, carcinoma, so-called cholemia, pregnancy, etc. (4) Prolonged 
drains upon the system, with loss of the albuminous constituents of the 
blood, such as occur in prolonged suppuration, nephritis, prolonged 
lactation, dysentery, etc. (5) Repeated hemorrhages — gastric and 



368 DISEASES OF THE HEMOPOIETIC SYSTEM 

duodenal ulcer, liver cirrhosis with hemorrhages, hemorrhoids, menor- 
rhagia, metrorrhagia, hemophilia, etc. (6) Inanition and starvation, 
due to deficient food or inability to swallow food, such as occur in oeso- 
phageal carcinoma and somewhat similarly in obstruction of the thoracic 
duct. (7) Insanity. In these latter cases the plasma often suffers much, 
and on account of inspissation the blood corpuscles may be relatively 
numerous (5,000,000 or more to the cubic millimeter). 

Symptoms. — In many cases the symptoms due to the anemia are inti- 
mately bound up with those due to the primary disorder, and it is difficult 
to separate the one from the other. In general, however, the symptoms 
of the anemia are those of general nervous and muscular irritability and 
weakness. The patient is readily fatigued by bodily or mental exertion, 
he is incapable of concentrated or continued mental effort, and headache, 
vertigo, syncopal attacks, tinnitus, dimness of vision, insomnia (or 
somnolence), are common, and occasionally nausea and vomiting may 
be present. The appetite is poor, the digestion often imperfect (vari- 
ability of HC1) and often painful (hyperesthesia of the gastric mucosa), 
and constipation is the rule (defective intestinal peristalsis). The heart's 
action is weak, though readily excited — whence palpitation and arrhyth- 
mia, as well as dyspnoea, are common; a systolic murmur is usually 
present, and a venous hum (bruit de diable) may be heard in the neck; 
the second pulmonary sound is accentuated; from dilatation, a relative 
mitral insufficiency may occur; the pulse is small, weak, and compres- 
sible, and the extremities are usually cool. Slight oedema, due to increased 
permeability of the vessels, occurs in some cases, and hemorrhages into 
the mucous membranes, under the skin, and in the retina and cerebral 
meninges are not uncommon. The urine is often increased in amount. 
Occasionally there is slight fever (anemic fever). There may be amenor- 
rhoea or menorrhagia; and perhaps impotence. 

The blood reveals oligocythemia (4,000,000 to 2,000,000), and dis- 
proportionate oligochromemia (65 to 30 per cent.); therefore a low color 
index (0.8 to ,0.6). In some cases, however, these figures are exceeded, 
and approach those of pernicious anemia. Microscopically, the cor- 
puscles are pale, and reveal anisocytosis, poikilocytosis, and polychroma- 
tophilia; nucleated corpuscles (usually normoblasts) may be present. 
There is little, if any, leukocytosis due to the anemia as such, but leu- 
kocytosis as a manifestation of the primary disorder is not uncommon. 

Diagnosis. — The diagnosis has to do not only with the recognition of 
the anemia, but also with its degree, and largely with its underlying dis- 
order. Cases of so-called simple anemia are usually chlorosis, pernicious 
anemia, tuberculosis, gastric carcinoma, neurasthenia, etc., and an effort 
should be made to differentiate these. 

Prognosis. — The prognosis is that of the primary causative factor. 

Treatment. — The treatment is primarily concerned with the detection 
and removal of the underlying cause. In addition, however, the patient's 
recovery may be materially aided by attention to the diet, and by suit- 
able medicines. The diet should be varied and nutritious, and should 



CHLOROSIS 359 

comprise a generous amount of red meats, milk, eggs, as well as other 
iron-containing articles, especially vegetables. Of medicaments, iron is 
of prime importance, and should be given in all cases. As a rule, no 
preparation is better than Blaud's pills, which should be given in generous 
doses (10 to 15 grains, 0.65 to 1 gram, three times a day); in some 
cases reduced iron, the dried sulphate or the citrate of iron, or Basham's 
mixture render excellent service. Arsenic is often a useful adjuvant, and 
may be given as Fowler's solution, 2 minims (0.12 c.c), three times a 
day. Occasionally bitter tonics and hydrochloric acid are indicated to 
improve the appetite, but hydrochloric acid had better be withheld unless 
we are certain that there is a deficiency of hydrochloric acid in the gastric 
juice. The following is often productive of excellent results : 

1$ — Reduced iron 80 grains 5 2 

Quinine sulphate 20 grains 1 3 

Strychnine sulphate 2 grains 13 

Arsenous acid 1 grain 06 

Mix and make 40 pills. 

S. — One pill three times daily. 

Minute doses of mercuric bichloride are sometimes serviceable, even in 
non-syphilitic cases. The debility of exhausting disorders, such as 
typhoid fever, prolonged lactation, neurasthenia, etc., is often much 
improved by the lactophosphates, the hypophosphites, cod liver oil, etc. 
In cases that do not respond promptly iron may be given hypodermicly, 
the citrate in doses of \ grain (0.03 gram) to children, 2 grains (0.13 gram) 
to adults, every other day. The bowels should be kept open once daily. 
Other suitable measures consist of medicated baths, massage, and change 
of climate — high altitudes being of undoubted service in some cases, 
since it seems that the increase in the corpuscular count obtained at 
high altitudes does not always disappear upon return to lower levels. 



CHLOROSIS. 

(Chloranemia; Green Sickness.) 

Chlorosis is a form of anemia occurring in young girls about the time 
of puberty, and characterized by marked oligochromemia and sometimes 
by a peculiar greenish tint of the skin. 

Etiology. — Chlorosis is peculiarly a disease of the female sex, occurring 
in blondes more frequently than in brunettes, and about the age of pu- 
berty, that is, from the fourteenth to the seventeenth year, but recurrences 
up to and probably beyond the twenty-fifth year are common. True 
chlorosis never occurs in males. It is most common among domestic 
servants and immigrants, particularly Irish; but if many chlorotic girls 
are underfed and overworked, have insufficient exercise and fresh air, 
many have been reared under the most favorable circumstances and do 
no work; if many have been subject to distressing emotional disturbances, 
such as worry, youthful love affairs, etc., others are unrestrained and 
24 



370 DISEASES OF THE HEMOPOIETIC SYSTEM 

free from care. The mothers of some chlorotic girls themselves were 
chlorotic about the age of puberty. 

The exciting cause of the disease is unknown — despite many hypoth- 
eses. Virchow attributed it to hypoplasia of the cardiovascular system, 
especially the aorta, and the genitalia; but these, though sometimes 
observed, can scarcely cause the disorder, since it is difficult to compre- 
hend the relationship between hypoplasia of the aorta and oligochrome- 
mia, since such hypoplasia does not cause chlorosis in boys, and whereas 
iron may cure chlorosis, it must be powerless to correct the hypoplasia. 
Sir Andrew Clark believed the disease to be a manifestation of intes- 
tinal auto-intoxication due to coprostasis — a view with little foundation 
in fact, since otherwise most girls and women would be chlorotic, and 
because evidences of intestinal putrefaction have not been found con- 
stantly in the urine of chlorotics. The occurrence of chlorosis in girls 
about the time of puberty suggests an intimate relationship between the 
series of changes then taking place and the alterations in the blood; 
possibly time may show that some derangement in the internal secretion 
of the ovary developing at the time the ovary begins to functionate 
actively, may be answerable for the disease. The majority of cases can- 
not be incipient pulmonary tuberculosis, as has been suggested, since 
they are readily cured with iron; nor is it likely that they are cases of 
more or less ill-declared hyperthyroidism, associated or not with tuber- 
culous lesions in the thyroid. Unquestionably chlorosis seems to be 
much less common than it was years ago, which is due to the fact that 
the causes of many chloranemic conditions are more commonly recog- 
nized ; this suggests the additional fact that chlorosis in reality is a sec- 
ondary anemia, of which the cause is not always demonstrable. The 
common absence of marked changes in the erythrocytes, the deficiency of 
pigments in the urine and feces, and the non-occurrence of even slight 
jaundice, suggest that the disease is due to defective hemogenesis rather 
than augmented hemolysis. 

Symptoms. — The symptoms, for the most part, are those of the con- 
comitant anemia, and as such do not differ from those described in con- 
nection with chronic secondary anemia. The early symptoms are usually 
breathlessness, palpitation of the heart (which too often suggests heart 
disease), vertigo, faintness, weariness of the mind and body without 
obvious cause, and indisposition to exertion. In marked contrast with 
the subjective complaints, the girl often presents a much prized though 
deceptive peach complexion (chlorosis rubra), especially Upon exertion or 
excitement, and she is more likely to be fat and round than thin and angu- 
lar. In marked cases, however, the skin exhibits the ordinary pallor of 
any secondary anemia; occasionally it presents a peculiar yellow-greenish 
color" most notable on the face, ears, dorsal surface of the hands, and the 
chest; pigment spots especially about the joints are often present; the 
eyes are bright, the conjunctivae transparent, and the sclerotics bluish. 
Indeed, the observing physician may usually make the diagnosis from 
mere inspection, and yet the disease is frequently overlooked. The 



CHLOROSIS 371 

appetite is often characteristically capricious, the patient evincing a liking 
for most extraordinary articles, such as chalk, paper, pickles, etc. (pica 
chlorotica) ; epigastric distress is common after eating, and constipation 
is the rule. Appropriate examination often reveals gastric hyperacidity, 
frequently gastroptosis and even gastrectasis (especially if the patient 
has succumbed to the vanity of tight lacing). Examination of the heart, 
suggested by the palpitation, usually reveals excited action; a systolic 
murmur, commonly with its point of maximum intensity toward the pul- 
monary area, though frequently audible over the entire precordium; a 
venous hum in the neck (bruit de diable); and often percussion evidence 
of enlargement (dilatation) of the heart. The murmur is usually 
attributed to anemia (and partakes of the characteristics of so-called 
anemic, functional, murmurs) ; in some cases, however, it is probably due 
to dilatation of the root of the pulmonary artery, and in some cases to 
relative mitral insufficiency (irregular action of the papillary muscles). 
Venous thrombosis (femoral, cerebral sinuses) is by no means uncom- 
mon (2 per cent, or more of the cases). The extremities are often cold 
(defective circulation). (Edema or puffiness of the feet and ankles is 
sometimes present, and has been mistaken for evidence of nephritis or 
heart disease. Divers nervous manifestations are common— headache, 
neuralgic pains in the neck and the back, and reflected elsewhere, 
general irritability and capriciousness, vulgar " hysterics," dermograph- 
ism and other evidences of vasomotor instability (or ataxia), etc. Slight 
fever occurs occasionally. 

The total volume of the blood is increased, due to increase of the plasma 
(serous plethora; polyplasmia), in consequence of which the vascular 
system is overdistended. The blood as it flows from the puncture is 
pale, but the characteristic feature is the marked reduction in the hemo- 
globin. The erythrocytes are often normal in number; they are usually 
over 4,000,000, that is, about 80 per cent, of the normal, whereas the 
hemoglobin varies from 35 to 65 per cent, in different cases, averaging 
about 40 per cent. The color index thus approaches 0.5. In some cases, 
however, there is quite a reduction in the erythrocytes — to 3,000,000 or 
2,500,000, or even less; but the disproportionate reduction of the hemo- 
globin (the low color index) is a constant feature. Microscopically the 
individual erythrocytes are pale (low color index, deficiency of hemo- 
globin), and anisocytosis (small cells) and poikilocytosis may be present 
and sometimes are marked (severe cases); large erythrocytes (mega- 
locytes), however, are rarely if ever seen; nucleated red cells are some- 
times present; polychromatophilia is rare. The leukocytes are usually 
normal in number, but a slight increase especially of the lymphocytes Is 
by no means unknown. 

Diagnosis.— As already stated, the diagnosis is often suggested by 
mere inspection of the patient, but the frequency with which the disease 
is overlooked and mistaken for something else is deplorable. If a hemo- 
globinometer is not at hand, recourse may be had to the simple device 
of comparing a drop of the patient's blood with a drop of presumably 



372 DISEASES OF THE HEMOPOIETIC SYSTEM 

normal blood, whereupon the deficiency of hemoglobin is immediately 
apparent. Care should be taken not to mistake beginning pulmonary 
tuberculosis for chlorosis, nor chlorosis for nephritis (on account of 
slight oedema), or heart disease (on account of palpitation and a murmur), 
or hyperthyroidism, or neurasthenia. The examination of the blood is 
usually conclusive, but one must bear in mind that a chloranemic con- 
dition of the blood is the unusual condition in secondary anemias. 

Prognosis. — The prognosis is good. Recovery, under proper treat- 
ment, ensues in from two to four or six months, but relapses are not 
uncommon, largely because of too early discontinuance of treatment. 

Treatment. — Rest in bed with an abundance of fresh air and sunlight, 
for a time at least, is advisable in all but the mildest cases. The food 
should be nutritious and generous in amount — milk, eggs, meats, fish, 
stewed fruits, green vegetables, etc.; but it is sometimes a tax on the 
patience of the physician to convince a chlorotic girl that she can digest 
food other than chalk and pickles, and that meat in particular will agree 
with her delicate stomach. Iron is a specific remedy. It is a matter of 
comparative indifference which preparation is given, provided the iron 
is given in generous amount. No preparation is better than Blaud's 
pills : 

I^ — Dried iron sulphate, 

Potassium carbonate, of each 100 grains. 6|6 

Mix and make 40 pills. 
S. — One pill three times a day for the first week, two pills three times a day for the second 
week, and three pills three times a day thereafter. 

The treatment must be persisted in for at least three months, despite the 
conviction of the patient that she is cured earlier, since otherwise recur- 
rence is almost inevitable. Under the influence of iron the erythrocytes 
soon reach the normal number, and while the hemoglobin value increases, 
considerable time is often required to attain the normal percentage. Ex- 
actly how the iron acts is a matter of speculation, and the theoretical 
objection to large doses, whereby more iron is given within a few days 
than is contained normally in the entire body, is not sustained by any 
clinical or experimental facts. Indeed, a markedly chlorotic patient, 
despite the evident need of iron in her blood, excretes iron in her feces, 
even before the administration of iron is commenced. Those who prefer 
them may use reduced iron, the citrate of iron and potassium, or the citrate, 
the dried sulphate, the pyrophosphate, the lactate, or the succinate of iron 
or the tincture of the chloride; one or the other of these may be given 
from time to time should convalescence prove tedious, in which case also 
minute doses of arsenic or of manganese may prove serviceable. The so- 
called organic preparations of iron, said to reproduce the normal iron of 
the body, are in no way superior, and in many ways inferior, to the 
preparations mentioned. 

In addition to the foregoing, the patient's bowels should be kept open 
daily — for which purpose, as a rule, nothing is better than the compound 
rhubarb pill (U. S. P.): 



PERNICIOUS ANEMIA 373 

T^— Rhubarb 48 g ra i ns 3 20 

Purified aloes 36 grains 2 40 

M y rrh 12 grains 80 

Oil of peppermint 4 m i n ; ms 25 

Mix and make 48 pills. 
S.- — One or two pills night and morning. 

Cascara sagrada, saline cathartics, phenolphthalein (1 to 2 grains, 0.06 
to 0.13 gram), etc., are also efficacious. Cleansing of the bowel should 
precede the beginning of the iron treatment. To patients with evident 
intestinal fermentation, it is wise to give for a time so-called intestinal 
antiseptics, especially bismuth salicylate, /?-naphthol, thymol, aspirin, 
preparations of the lactic acid bacillus, etc. In other patients with imper- 
fect digestion, hydrochloric acid, nux vomica, and the bitter tonics prove 
efficacious; but one must remember that hyperchlorhydria is common in 
chlorosis. 



PERNICIOUS ANEMIA. 

Pernicious anemia is a chronic disease of the hemopoietic tissues 
characterized by hemolysis of unknown cause, abnormal hemogenesis, 
and alternating periods of remission and relapse.. 

There has been and there still is much discussion as to what is and 
what is not properly pernicious anemia. There are several disorders 
that may give rise to clinical and blood pictures resembling, if not quite 
identical with, pernicious anemia that should be excluded, since they are 
obviously secondary anemias of severe (perhaps one might say also 
pernicious) and even fatal type. These include: (l),Some cases due to 
severe and frequently repeated hemorrhages; (2) certain cases of severe 
malarial, syphilitic, and other infections; (3) Dibothriocephalus latus and 
other zooparasite infections, in which the blood picture may be quite 
identical with that of pernicious anemia and the termination fatal; 

(4) cases of severe and fatal anemia occurring during pregnancy or soon 
after parturition, and due presumably, as is the vomiting, nephritis, and 
eclampsia of pregnancy, to some auto-intoxication, or to puerperal 
hemorrhage or infection; these occur, as a rule, in young subjects (thirty 
to thirty-five years), do not show the remissions characteristic of per- 
nicious anemia, and are often curable upon removal of the initiating cause; 

(5) cases due to primary changes in the bone marrow, such as primary 
or secondary tumor formation, or leukemia (so-called myelophthisic 
anemia). There remains a series of cases of unknown cause to which 
the term pernicious, idiopathic, essential, Addison's, or Biermer's anemia 
may be applied. 

Etiology. — Pernicious anemia is especially common in adult life: more 
than half the cases occur after the fortieth year; it is rare in childhood. 
It is more than twice as common in men as in women (eliminating the 
cases occurring in pregnancy). The cause of the disease is not known. 
It has been variously attributed to nervous shock; to repeated or long- 



3^4 DISEASES OF THE HEMOPOIETIC SYSTEM 

continued, perhaps concealed, gastro-intestinal hemorrhages (which are 
more likely a result than a cause of the disease); to atrophy of the 
gastro-intestinal mucosa (which, however, is not always present, and if 
present may as well be a result as a cause, or a manifestation of the 
same cause); to subinfection with intestinal bacteria; and, especially 
by Hunter, to oral and gastro-intestinal sepsis. Hunter states that the 
disease is a well characterized specific infective disease of hemolytic 
nature localized in the alimentary tract; that in its etiology long-standing- 
sepsis, oral and gastric, plays an essential and important antecedent 
and concurrent part; that anemia is but one of the symptoms, of which 
there are three others: (1) Glossitic and gastro-intestinal; (2) hemo- 
lytic; and (3) febrile and nervous — far more characteristic and due not 
to the anemia, but to the infective agencies underlying the disease. Dis- 
approving of the term pernicious, he separates this so-called Addisonian 
(primary cryptogenetic) anemia, a specific infective disease, sharply from 
other types of severe or pernicious (Biermer's) anemia, which he believes 
may be due to other types of general sepsis; and all these types, which he 
characterizes as infective anemias, he differentiates from so-called non- 
infective anemias — that is, chlorosis and all the ordinary posthemorrhagic 
and other types of secondary anemia. 

Pathology. — The conspicuous lesions consist of pallor, a lemon tint, 
or even slight jaundice of the skin; pallor of all the viscera; a peculiar 
bright red color of the muscles and light yellowish fat; fatty degeneration 
of the liver, heart, and kidneys (toxic, perhaps, rather than anemic degen- 
eration); petechial hemorrhages in the subcutaneous, submucous, and 
subserous tissues; effusions in the serous sacs; systemic or disseminated 
degeneration of the posterior columns, and sometimes of the lateral 
columns and of the gray matter of the spinal cord (perhaps also toxic 
rather than anemic). Hunter emphasizes the importance of certain 
so-called infectious lesions; a peculiar glossitis, gastritis or gastric 
atrophy, and patchy enteritis, which he believes to be insufficient in 
themselves to originate the intense anemia by an interference with nutri- 
tion. The liver, spleen, lymph nodes, and hemolymph nodes usually 
show considerable deposit of blood pigment and large numbers of 
phagocytes (macrophages) containing more or less completely destroyed 
erythrocytes — all evidences of excessive hemolysis. The fatty portions 
of the bone marrow are usually more or less replaced by red marrow 
resembling the fcetal or juvenile type (megaloblastic degeneration or 
metaplasia), interpretable as an effort to compensate for the excessive 
hemolysis; there may be also some evidences of leukoblastic hyperplasia. 
In some cases the bone marrow is either incapable of responding or 
ultimately becomes exhausted, whereupon it may be more or less com- 
pletely yellow (fatty) throughout (aplastic anemia). 

Symptoms. — The disease, as a rule, is exceedingly insidious in onset, 
and it often has made considerable progress, that is, the blood is remark- 
ably bad, when the patient first seeks medical advice. The initial mani- 
festations are variable and permit of some grouping of the cases: (1) 



PERNICIOUS ANEMIA 375 

Gradually increasing weakness, especially upon exertion, with dyspnoea 
and palpitation of the heart; (2) gastro-intestinal derangements— sore 
mouth, anorexia, nausea, vomiting, diarrhoea, or perhaps constipation; 
(3) general nervous irritability or inadequacy, lost power of mental 
effort or concentration, headache, vertigo, tinnitus, fainting, somnolence, 
cutaneous parasthesias and ataxia, spasticity of the muscles of the legs, 
etc. In the course of time the symptoms become aggravated. The 
weakness and weariness increase; mental effort and concentration are 
even less well sustained than previously; and dyspnoea and palpita- 
tion of the heart become more marked. Hemorrhages (usually pete- 
chial) may occur into the skin, visible mucous membranes, retina, etc.; 
nausea and vomiting may become aggravated, and are often associated 
with paroxysmal attacks of epigastric pain and diarrhoea. In a majority 
of the cases nervous phenomena become more or less obtrusive, such as 
various paresthesias, numbness, tingling, etc. (even in the absence, of 
demonstrable changes in the spinal cord); in other cases symptoms 
suggestive of tabes dorsalis (severe pains, absent knee-jerks, etc.) occur; 
they may even precede and ultimately become more marked than symp- 
toms referable directly to the anemia; in other cases, spasticity of the 
muscles of the legs and increased knee-jerks, associated late, perhaps, with 
incontinence of urine and feces, supervene. To a not uncommon mental 
apathy a depressive psychosis (melancholia) sometimes succeeds. 

On examination the patient may present a general cutaneous pallor, 
such as might be encountered in any severe anemia; in other cases there 
is a characteristic waxy, lemon-yellow color of the skin; in some cases 
there is even slight jaundice (not as frequent as is often diagnosticated); 
and rarely there is more or less pigmentation (and perhaps associated 
leukoderma), suggesting Addison's disease. The subcutaneous fat is 
usually well preserved, and there is often comparatively little loss of 
weight. As a rule, there is a notable absence of abnormal physical signs. 
The heart is usually somewhat dilated; there may be hemic murmurs 
over the heart and in the cervical veins, or a murmur of relative mitral 
insufficiency; the pulse may be full but not well sustained; the blood 
pressure is usually low (often less than 100 mm. Hg., systolic or maximum) ; 
and a capillary pulse may be visible. (Edema of the legs and hands is 
common, and transudations may occur into the pleura, peritoneum, 
etc. The spleen and liver may be slightly enlarged; occasionally also 
the palpable lymph nodes. Hydrochloric acid and the digestive ferments 
are usually absent or greatly diminished; there is rarely any marked 
dilatation of the stomach or motor insufficiency except perhaps at the 
time of the paroxysmal pains. The urine is usually pale and of Low 
specific gravity; in from one-fourth to one-half of the cases it contains a 
small amount of albumin and perhaps a few casts; occasionally it is dark 
in color, due usually to an excess of urobilin. Fever occurs in about three- 
fourths of the cases— often (100° to 102°) for a week or two at a time. 

The blood is abnormally fluid, and the total volume is lessened. The 
red cells are remarkably reduced, numbering often 2,000,000 or less 



376 DISEASES OF THE HEMOPOIETIC SYSTEM 

when the patient first consults a physician — which in itself suggests the 
disease; later they may fall to 1,000,000 or less (even 143,000, Quincke). 
The color index is high, 1.0 to 1.5 or more (often increasing with the 
progress of the disease and lessening during the periods of remission); 
this is characteristic of the disease, and attributable not to hemoglo- 
binemia (which, however, is occasionally present), but to the large number 
of macrocytes rich in hemoglobin. Poikilocytosis is usually extreme; 
there is marked anisocytosis, megalocytes being present usually in such 
size and numbers as to increase the average diameter of the erythro- 
cytes (offsetting the lessened diameter of the microcytes); polychroma- 
tophilia (diffuse and granular) is exceedingly common (more so than in 
any disease other than lead poisoning); and nucleated red corpuscles, espe- 
cially megaloblasts, are present in more than 90 per cent, of the cases. The 
leukocytes are usually diminished (5000 or less) — usually a polynuclear 
deficit; there may be a relative, sometimes an absolute, lymphocytosis. 
Sometimes the leukocyte count is normal, especially during the remis- 
sions; rarely there is a slight leukocytosis (blood crisis; complicating, 
perhaps, terminal infection). A few myelocytes are often encountered. 
The blood platelets are lessened. Often what are spoken of as blood 
crises occur — sudden increase of the erythrocytes (50 or more per 1000 
leukocytes), and of the leukocytes (especially the eosinophiles). The crises 
may be spoken of a normoblastic or megaloblastic, depending upon the 
predominating type of nucleated cell. These often are favorable signs 
of bone-marrow activity and are followed by general and blood improve- 
ment; but sometimes they represent the final effort of an exhausted 
marrow and may portend an early fatal issue. 

A characteristic of the disease is alternating periods of remission and 
relapse — which often succeed each other with considerable regularity. 
As a matter of fact, when the blood is poor it is remarkably inconstant, 
the erythrocyte count either increasing or diminishing. A total count of 
over 4,000,000 is rarely attained; but the blood may remain stationary 
at a good, rather high level for from two to six, sometimes six to twelve, 
months or more. Considerable improvement as well as deterioration of 
the blood not infrequently occurs without noteworthy change in the 
general subjective complaints of the patient; these (as well as the fatty 
degeneration of the viscera and the lesions in the spinal cord) likely are 
due in part only to the anemia as such, and in part to the underlying 
(toxic?) factor. 

Diagnosis. — The diagnosis should be made more frequently than it is, 
and might readily be made by attention to Addison's statement that it is 
a disease "occurring without any recognizable cause whatever; where 
there has been no previous loss of blood, no exhausting diarrhoea, no 
chlorosis, no purpura, no renal, splenic, glandular, strumous, or malig- 
nant disease, . . . and without any organic lesion that could 
properly or reasonably be assigned as an adequate cause of any serious 
consequences." In addition to the phenomena common to any severe 
anemia, the following are significant of pernicious anemia : Severe cause- 



PERNICIOUS ANEMIA 377 

less anemia in a middle-aged or elderly male subject; generally well-pre- 
served panniculus adiposis with little loss of weight; sore mouth; par- 
oxysmal attacks of epigastric pain often attended with diarrhoea; retinal 
and other hemorrhages; extraordinarily low erythrocyte count at the 
first examination, that is, the patient's general good appearance is in 
notable contrast to the condition of his blood, and he is often able to 
continue at his work with an erythrocyte count approaching 1,000,000; 
high color index; normal leukocyte count or leukopenia; an unusually 
large number of megalocytes (over 30 per cent, of the total erythrocyte 
count being quite diagnostic), megaloblasts, and poikilocytes; poly- 
chromatophilia ; and alternating periods of remission and relapse. All 
types of severe secondary anemia may be excluded by the detection of a 
causative factor, especially severe and frequently repeated hemorrhages, 
pregnancy, severe infections, intestinal parasitism (ova in the stools), 
etc. Gastric carcinoma, myxcedema, etc., sometimes bear a more or less 
superficial resemblance to pernicious anemia, but with ordinary care they 
should be readily excluded. 

Aplastic anemia virtually is only an extremely severe and rapidly 
fatal form of pernicious anemia, characterized by slight if any response 
on the part of the bone marrow to the demand for erythrocytes. The 
marrow of the long bones is yellow throughout — aplastic (rather than 
hyperplastic or metaplastic) as contrasted w T ith the ordinary type of 
pernicious anemia. It is a disease that especially affects young women 
before the thirty-fifth year; subcutaneous and submucous hemorrhages 
are more common; it is steadily progressive, showing none of the char- 
acteristic remissions; and it usually leads to death within a few months 
(three or thereabouts). The blood is characterized by the common 
extraordinary oligocytosis, but the color index is likely to be low (0.8); 
erythroblasts are usually absent and so-called erythroblastic crises do not 
occur; poikilocytosis, anisocytosis, and polychromatophilia are less 
marked than in the ordinary type of pernicious anemia; there is marked 
leukopenia, due largely to a loss of granular leukocytes, so that most 
(75 to -90 per cent.) of the white cells are lymphocytes; and the blood 
platelets are markedly lessened. 

Leukanemia is a term given by Leube to a blood state that combines 
some of the features of pernicious anemia and of leukemia, especially 
megaloblasts, myelocytes, and lymphocytes. The majority of the cases 
can, with little difficulty, be classified as pernicious anemia, on the one 
hand, or leukemia, on the other; in the terminal stages of both of those 
diseases blood findings significant of the other are not rare. 

Prognosis. — The disease usually, if not invariably, runs a fatal course in 
from one to three years; occasionally, as in aplastic anemia, within a few 
months; perhaps rarely it continues for five or more years with uncom- 
monly long periods of remission. Death usually ensues from progres- 
sively increasing weakness, oedema of the lungs, or terminal infections. 

Treatment.— The essentials of treatment comprise prolonged resl 
(mental and physical), an abundance of fresh air, and good, nutritious, 



378 DISEASES OF THE HEMOPOIETIC SYSTEM 

readily digestible food (especially milk and vegetables, but not too much 
nitrogenous food); and the administration of arsenic and hydrochloric 
acid. Arsenic seems to act by stimulating the erythroblastic centres in the 
bone marrow. It should be given cautiously, in gradually increasing doses, 
to the point of toleration (epigastric pain, nausea, vomiting, diarrhoea, 
puffiness and itching or burning of the eyelids, etc.). Arsenous acid, 
Fowler's solution, or sodium cacodylate, may be given. In some cases 
good results follow hypodermic administration : sodium cacodylate, \ grain 
(0.008 gram) , iron citrate, 2 grains (0.13 gram), daily or every second day. 
Hydrochloric acid is indicated on account of the gastric achylia, but it is 
said to have also other beneficial effects. Particular attention should be 
paid to the teeth and mouth. The services of a dentist are often of the 
greatest utility. Antiseptic mouth washes should be used. Lavage of the 
colon also is serviceable, especially in the event of indicanuria and other 
evidences of supposed intestinal decomposition. Hypodermoclysis with 
physiological saline solution also has been commended. Cholesterin (3 per 
cent, solution in hot olive oil, 100 c.c. daily) has been recommended with a 
view to combining a hemolysin in the blood, which is believed to rob the 
erythrocytes of their cholesterin and lead to hemolysis, analogous to the 
action of cobralecithin. Large amounts of milk, cream, and butter tend 
to achieve the same object. Red bone marrow has fallen into disuse; by 
some its occasional good results have been attributed to the glycerin 
contained in the commonly used preparation — the glycerin extract. 



LEUKEMIA. 

(Leukocythemia.) 

Leukemia is a disease of the hemopoietic system, characterized by 
hyperplasia of the leukoblastic tissues and by marked and usually per- 
manent increase in the number of circulating leukocytes. 

The older writers described three types of leukemia — the splenic, the 
lymphatic, and the medullary; but under the influences of Ehrlich these 
became merged into two, the splenomedullary and the lymphatic — 
which were held to be sharply differentiated the one from the other. 
The one, the lymphatic type (lymphemia), was believed to be due to 
primary disease of the lymph nodes; the other, the splenomedullary 
or myelogenous type (myelemia) was believed to be due to primary 
disease of the bone marrow. But with the determination of the fact that 
a number of cases of lymphatic leukemia occur with slight or no note- 
worthy changes in the lymph nodes, and that in all cases of leukemia 
more or less conspicuous changes occur in the bone marrow, the possi- 
bility of all cases of leukemia being myelogenous seemed proved. 

The data now at hand warrant the opinion that leukemia is a disease 
of the leukoblastic tissues throughout the body — the bone marrow, the 
spleen, and the lymph nodes; that the process may begin in either the 
bone marrow or the lymph nodes (it is not likely that it ever begins in the 



LEUKEMIA 379 

spleen); that in some cases the lesions are most marked in the bone 
marrow, in others in the lymph nodes, but that changes are always 
present in the bone marrow; that, depending perhaps upon the nature 
of the initiating (chemotactic ?) factor, the leukoblastic proliferation in 
one series of the cases is of the lymphocytic or lymphoid type, and gives 
rise to a large number of circulating lymphocytes, whereas in another series 
of cases it is of the myelocytic or myeloid type, and gives rise to a large 
number of circulating myelocytes; and that the essence of the process is 
a reversion to the more or less undifferentiated leukoblastic tissue of 
foetal life. This is suggested by the fact that the circulating lymphocytes 
and myelocytes of leukemia differ materially from the normal circulating 
lymphocytes and bone-marrow myelocytes (reversion to a common 
ancestral type ?), and by the fact that the process, whether myeloid or 
lymphoid, soon involves in similar metaplasia tissues other than that 
where it originated; that is, the bone marrow may become converted 
into lymphoid tissue, or the lymph nodes and the spleen may become 
converted into myeloid tissue — these respective changes being metaplasias 
rather than the result of the proliferation of so-called metastases. 

The foregoing facts permit of the differentiation of the cases into two 
main types: (1) Myelocytic or myeloid (splenomedullary), and (2) 
lymphocytic or lymphoid. In some respects these represent extremes of 
type rather than distinct diseases; some cases do not fit well into either 
group, and may be spoken of as atypical (transitional, intermediate, or 
mixed) forms. 

Etiology. — The cause and the nature of the disease are not known. 
Many, especially the acute, cases run a course strongly suggesting an 
infection, but no infectious agent has yet been discovered, if one excepts 
Spirochseta lymphatica (White and Proescher), which still awaits con- 
firmation. Warthin and others are inclined to look upon the disease as 
allied to the tumor formations, believing that transitions occur from leu- 
kemia through myeloma to ordinary sarcoma. In some cases there is a 
history of antecedent infections, such as malaria, syphilis, typhoid 
fever, tonsillitis, puerperal and other types of septicopyemia, etc.; but in 
most of the cases the supposed infection is in reality the declared, although 
not diagnosticated, leukemia. 

Myelocytic or Myeloid Leukemia. — Myelocytic or myeloid leu- 
kemia, the most common form, occurs especially in males (two-thirds of 
the cases), and is most common in the fourth and fifth decades (60 per 
cent, of the cases). 

Pathology. — The lesions consist of myelocytic hyperplasia of the leu- 
koblastic tissues of the bone marrow and of myelocytic (or myeloid) 
metaplasia of the spleen and perhaps also of the lymph nodes. The 
marrow, especially of the long bones, but also of the ribs, vertebra', 
sternum, etc., becomes converted into a reddish or grayish-red tissue, 
and the fatty marrow of the long bones gradually disappears. The 
spleen becomes enlarged, and may weigh 4000 to 6000 grams or more; 
its shape is preserved; it varies in consistency with the amount of sclerosis ; 



380 DISEASES OF THE HEMOPOIETIC SYSTEM 

on section it usually much resembles the associated bone marrow, but 
it may show areas of infarction, hemorrhage, or sclerosis. The liver also 
becomes enlarged, and may weigh as much as the enlarged spleen, or 
more. The lymph nodes throughout the body (the superficial and deep 
chains, the hemolymph nodes, the tonsils, etc.) also may be, but are not 
always, enlarged. Microscopically the bone marrow and the spleen 
exhibit myeloid transformation — myelocytes and cells derived therefrom 
(all the granular leukocytes), mononuclear cells (perhaps ancestors of the 
myelocytes), megakaryocytes (with divers sorts of inclusions), erythro- 
cytes and erythroblasts in various and atypical stages of development, 
etc. Similar changes may be found also in the lymph nodes. The 
capillaries of the liver, kidneys, lungs, etc., are overfilled with similar 
cells, and there are sometimes extra-capillary collections, and degenera- 
tion of the parenchymatous cells. 

Symptoms.— The onset of the disease is insidious: the patient may 
seek advice on account of progressive loss of flesh and strength, the dis- 
comfort occasioned by a large mass in the region of the spleen, various 
gastro-intestinal disturbances, dyspnoea and palpitation of the heart, 
especially on exertion (and other evidences of anemia), or a sudden, 
perhaps serious hemorrhage. Anemia is not an early symptom, but 
becomes marked as the disease advances, and is attended by the usual 
symptoms. Hemorrhages occur in 80 per cent, of the cases: epistaxis 
is the most common; but frequently there is bleeding from the gums, 
the stomach, the intestine, the uterus, etc.; into the skin (purpuric and 
ecchymotic spots), in the retina (blindness), into the brain (hemiplegia, 
etc.), and into the serous cavities. The first hemorrhage is sometimes 
severe and fatal. Gastro-intestinal disturbances (anorexia, nausea, 
vomiting, diarrhoea, etc.) are sometimes marked, and have been found 
with unusual (sometimes ulcerated) lesions in the intestines. Occa- 
sionally there is more or less marked dyspnoea, due in part, perhaps to 
myeloid deposits in the lungs and the respiratory mucosa. Hemorrhage 
or myeloid nodes may cause dimness of vision or blindness if they occur in 
the retina or optic nerve or disk; exophthalmos, if in the orbit; deafness, or 
Meniere's disease, if in the semicircular canal, etc. Priapism is occasion- 
ally a distressing symptom. Fever (102° to 104°) occurs from time to time 
in almost if not quite all cases. Toward the end evidences of anemia often 
become ascendant — dyspnoea, palpitation, oedema, and other evidences of 
cardiac weakness and dilatation. 

Examination reveals a greatly enlarged spleen — which may reach far 
beyond the median line and into the pelvis; it is usually hard, but some- 
times painful and tender; it reveals distinct notching; often it progres- 
sively increases in size, but when very large it may remain stationary, 
and it may become smaller after a severe gastro-intestinal hemorrhage or 
diarrhoea, or in consequence of progressive sclerosis. The liver also is 
usually enlarged; and the superficial lymph nodes may be palpably 
enlarged. The bones may be tender to percussion. The urine contains 
a great excess of uric acid (more than in any other disease), due to 



LEUKEMIA 3Si 

destructive katabolism of nucleins (of the leukocytes). In a majority of 
the cases it contains also at least a small amount of albumin and perhaps 
a few casts. 

The conspicuous feature of the disease is the great increase in the 
number of circulating leukocytes. They usually vary from 100,000 to 
500,000 when the patient first seeks advice; commonly there is a pro- 
gressive, though not steady, increase in their number, so that counts of 
1,000,000 or more are not rare. This increase is due to an absolute 
increase of all the normal circulating leukocytes (including lymphocytes) 
and to a large number of myelocytes. The myelocytes and the polynuclear 
neutrophils each vary, as a rule, between 30 and 60 per cent, of the total 
leukocytes, the polynuclear neutrophils being usually in excess of the 
myelocytes; the eosinophils and the basophiles (mast cells) also show 
a percentage as well as an absolute increase; the lymphocytes and the 
so-called large mononuclear leukocytes (variously named), as a rule, 
show no percentage increase (usually a percentage decrease), but a great 
absolute increase. All of the leukocytes (including the myelocytes) 
exhibit various deviations from the normal in size, shape, character of 
the nucleus, and staining affinities of the protoplasm and of the granules. 

The red cells may not be much reduced until the disease has made 
considerable progress, when marked oligocythemia may occur — 2,000,000 
or less; so that in advanced cases the ratio of leukocytes to erythrocytes 
may be 1 to 2, even 1 to 1. The color index is usually low (0.8 or less), 
as in any secondary anemia. Normoblasts and megaloblasts are always 
present; they are often polychromatophilic, and may exhibit mitosis. 
The blood platelets are increased. Charcot-Leyden crystals often sepa- 
rate out from the clotted blood. 

Lymphocytic or Lymphoid Leukemia. —Lymphocytic or lymphoid 
leukemia (lymphemia) is relatively uncommon, and occurs mostly in 
males (two-thirds of the cases). The acute cases are most common 
before the thirtieth year, many occurring before the twentieth year; 
the chronic cases are most common after the thirtieth, especially after 
the fiftieth year (80 per cent, of the cases). 

Pathology. — The lesions consist of lymphocytic or lymphoid hyper- 
plasia of the leukoblastic tissues — the lymph nodes, the spleen, and 
the bone marrow. The changes likely may begin anywhere in the leuko- 
blastic tissues, but the bone marrow apparently is always involved; in 
some cases the lymph nodes show no changes whatever. The naked eye 
appearances are not notably different from those seen in myelocytic 
leukemia; but microscopically the cellular infiltrations and nodule 
formations are of the lymphoid type (large or small cell, depending 
largely upon the acuteness or chronicity of the process). 

Symptoms. — The onset may be abrupt or insidious. The acute cases 
exhibit the common phenomena of an acute infection, with fever (104° to 
107°), and its common concomitants, weakness, progressive emaciation, 
etc. Often the cases are mistaken for typhoid fever, puerperal infection, 
other types of septicopyemia, etc. Usually there is moderate enlarge- 



382 DISEASES OF THE HEMOPOIETIC SYSTEM 

ment of the palpable lymph nodes, but this may be totally wanting, or 
it may supervene late in the course of the disease. In some cases the 
early complaint is of enlarged tonsils, which is usually misinterpreted 
as tonsillitis (confirmation of this supposition being sometimes found 
in enlargement and tenderness of the adjacent cervical lymph nodes, the 
fever, and leukocytosis — without a differential count). Hemorrhages are 
quite characteristic, and with the other phenomena suggest the disease 
even without a blood examination. The hemorrhages occur into the skin 
(petechias, ecchymoses), in the mucous membranes, especially the mouth, 
gastro-intestinal tract, genito-urinary tract, etc.; in the serous mem- 
branes, the retina, the viscera, etc.; often, especially in the mouth and 
the gastro-intestinal tract they are attended by much ulceration and 
sloughing. The chronic cases usually begin with increasing weakness 
and enlargement of the lymph nodes — the cervical, the axillary, the 
inguinal, etc. In some cases there is at first marked enlargement which 
has developed rapidly, but this gradually subsides and the disorder then 
goes on chronically; but in some cases, in the absence of glandular enlarge- 
ment, the diagnosis is first disclosed by an examination of the blood. 
Hemorrhages are uncommon in the chronic cases. Attacks of fever 
may occur from time to time. 

Examination discloses much the same abnormal physical conditions 
as are encountered in myelocytic leukemia. The palpable lymph nodes, 
as a rule, are more or less, sometimes enormously, enlarged (in contrast 
to the usual slight enlargement in myelocytic leukemia); the mesen- 
teric and retroperitoneal nodes may be palpable; the spleen and the 
liver, however, are rarely as enlarged as in myelocytic leukemia. The 
skin, in addition to hemorrhages, may disclose urticarial swellings, 
lymphomatous nodules, etc. 

The diagnostic feature of the disease is the great increase of circu- 
culating lymphocytes. The total leukocyte count varies from normal to 
500,000 or more; usually at the first count it varies between 20,000 and 
60,000; the average is less than in myeloid leukemia (about 150,000 as 
compared to about 400,000), but rarely in very acute cases the count 
may exceed that of the myelocytic variety. The increase consists exclu- 
sively of lymphocytes, which may constitute 99 per cent, or more of the 
total count. The acute cases usually reveal a very high total leukocytic 
count, high percentage of lymphocytes (90 to 99 per cent.), and pre- 
ponderance of large lymphocytes; the chronic cases, less high total 
count, less percentage of lymphocytes (50 to 80 per cent, or more), and 
preponderance of small lymphocytes. The small lymphocytes doubtless 
are derived in large measure from the lymph nodes ; but the large lympho- 
cytes of leukemia seem to be unquestionably bone-marrow cells, since 
they differ materially from the normal large lymphocytes of the cir- 
culating blood, and much resemble, if they are not identical with, cells 
variously described as Grawitz's unripe or immature leukocytes, indif- 
ferent lymphoid cells (Pappenheim and Wolff), Naegeli's myeloblasts, 
Turk's stimulation cells, etc.; perhaps they are in reality mother cells, 



LEUKEMIA 383 

and to be interpreted as manifestations of reversion to an ancestral type. 
Some of the small lymphocytes also are distinctly of this type, 'and 
often there is no sharp line of distinction between the so-called large 
and the small lymphocytes. The lymphocytes occasionally exhibit mitotic 
figures; commonly they show divers retrograde changes. The granular 
leukocytes are relatively and absolutely reduced; one or the other type 
may be entirely absent from time to time. Occasionally a few myelo- 
cytes may be seen (stimulation myelocytosis). The erythrocytes usually 
are reduced to between 3,000,000 and 4,000,000 when the patient is 
first seen; the color index is low, and there are the other evidences of 
secondary anemia — which increase with the progress of the disease. 
Erythroblasts are usually present, especially in the acute cases. 

Atypical Leukemia. — The term atypical leukemia finds some, but 
incomplete, justification in certain deviations from the common types 
exhibited by the two varieties of leukemia and in the occurrence of cer- 
tain disorders more or less resembling leukemia, or out of which leu- 
kemia may develop. In otherwise typical leukemia, the blood picture 
is sometimes atypical; thus, the typical picture of lymphocytic leukemia 
may be present with a total leukocyte count of 7500 or less; in myelo- 
cytic leukemia the eosinophiles or mast cells may be absent or unusually 
numerous, and the percentage of polynuclear neutrophiles may be very 
high or very low; and under the influence of infections, such as influenza, 
miliary tuberculosis, etc., the leukemic blood picture may become 
remarkably altered, or it may disappear entirely temporarily. The blood 
picture often becomes atypical shortly before death. In some cases 
leukemic or leukemic-like changes occur in the hemopoietic tissues 
without leukemic changes appearing in the circulating blood (discussed 
under tumors and tumor-like formations of the lymph nodes); in some 
of these cases true leukemia with the characteristic blood picture may 
subsequently develop. Rarely leukemic changes have been found in 
the blood without leukemic changes in the hemopoietic tissues (doubt- 
less due to imperfect examination). The supposed association of some 
features of leukemia with some features of pernicious anemia (leukanemia, 
Leube) has already been mentioned. Only rarely, and then doubtfully, 
do any of these conditions justify the term atypical leukemia. 

Chloroma. — Chloroma is an atypical form of lymphocytic leukemia in 
which the leukoblastic hyperplasias take on a greenish tint and in which 
some of those growing in the bone marrow penetrate the bone and give 
rise to veritable tumor formations that invade the surrounding tissues. 
The tumor-like growths are found most commonly in the skull, orbit, 
ribs, sternum, vertebrae, etc., but also in the long bones and in the 
lymph nodes, the viscera (kidneys, liver, spleen), the skin, etc. They give 
rise to local pain (headache, pains in the legs, etc.), regional swellings 
(especially in the temporal region, the orbit, etc.), deafness, exophthal- 
mos, blindness, etc. The general manifestation, such as weakness, 
emaciation, hemorrhages, anemia, enlargement of the lymph nodes, the 
spleen, and the liver, and the blood picture are quite like those of Ivmpho- 



384 DISEASES OF THE HEMOPOIETIC SYSTEM 

cytic leukemia; rarely they have been said to resemble myelocytic 
leukemia. The disorder is usually fatal within four or six months; 
occasionally it has been protracted to a year or more. 

Diagnosis. — The diagnosis of leukemia is often suggested by enlarge- 
ment of the spleen or the lymph nodes (especially significant if associated 
with hemorrhages), but certainty is obtained only by an examination of 
the blood. One should distinguish between acute and chronic cases: 
myelocytic leukemia is almost always chronic; lymphocytic leukemia 
may be acute (large cell variety) or chronic (small cell variety). Acute 
cases are also characterized by fever, hemorrhages, and marked fluctu- 
ation in the number of circulating leukocytes and in the size of the 
enlarged lymph nodes and the liver and the spleen. One must exclude 
typhoid fever, which the acute cases resemble in the fever, typhoid state, 
enlarged spleen, perhaps intestinal hemorrhages (and the ulceration of 
Peyer's patches that may be found after death). Different types of 
septicopyemia (acute endocarditis, puerperal infection, liver abscess, 
etc.), scurvy, hemorrhagic purpura, etc., also must be excluded; in 
many cases the diagnosis is not possible without an examination of the 
blood. The lymphocytosis that sometimes occurs in certain infectious 
diseases, notably pertussis, but also syphilis, malaria, etc., and the 
myelocytosis that may occur in infections, such as diphtheria, scarlatina, 
etc., and in certain forms of secondary anemia (notably von Jaksch's 
disease), should not be confused with leukemia. Care should be taken 
also not to overlook the disease in the beginning when the leukocytosis 
may be very slight, or later, during a period of remission, when there 
may be a fall to almost, if not quite, the normal number of leuko- 
cytes; a differential count will furnish the clue to the correct diagnosis. 
The differentiation from Hodgkin's disease and other disorders attended 
with enlarged lymph nodes is discussed under tumors and tumor-like 
formation of the lymph nodes. 

Prognosis. — The disease is always fatal — within a week to two or three 
months in the acute cases ; within from six months to three or more 
years in the chronic cases. In the acute cases death usually ensues in 
consequence of fever, hemorrhages, anemia, and exhaustion. In the 
chronic cases, remissions for weeks or months are not uncommon (spon- 
taneous or due to intercurrent infection, treatment, etc.). Death may 
result from the ordinary progress of the disease, which toward the end is 
likely to be rapid, or from an intercurrent infection, such as tuberculosis, 
pyococcic infection, influenza, pneumonia, etc. 

Treatment. — The nature of the disease, so far as we know, seems to 
preclude effective treatment. The acute cases pursue, as a rule, a steadily 
progressive course to the fatal issue, although rarely a case beginning 
apparently acutely becomes stayed and goes into the chronic stage. In 
the chronic cases arsenic and the x-rays are often of much benefit — 
arsenic in both varieties of the disease, the x-rays especially in the myelo- 
cytic variety. The arsenic should be given in gradually ascending doses 
to the point of toleration; sometimes benefit is not apparent until the 



ERYTHREMIA 385 

dose reaches a dram of Fowler's solution daily. The x-ray treatment 
should be carried out as recommended by Stengel and Pancoast systemati- 
cally : the bone marrow in different regions in succession should be sub- 
jected to the action of the ^-rays for periods averaging fifteen minutes 
daily; the spleen should not be subjected to the direct action of the 
arrays until it has become reduced in size and the total leukocyte count 
has diminished; special care must be exercised to avoid even the slight- 
est toxic reaction. The treatment should be continued until the spleen 
and the leukocyte count are normal; discontinuance of the treatment 
should be gradual, and the period of cessation should not be too pro- 
tracted. The arrays exert a specific leukolytic action, especially on the 
young cells — the non-granular mononuclear leukocytes and the myelo- 
cytes; and the serum of a leukemic subject that has improved under 
x-yslv treatment contains a substance which injected into lower animals 
produces leukopenia, disintegrating, first, the mononuclear cells; perhaps 
the future will furnish us a leukolytic serum efficient in human subjects. 
Splenectomy in leukemia, of course, is an irrational measure. 



ERYTHREMIA. 

(Erythrocytosis ; Megalosplenic Polycythemia or Erythrocythemia ; Polycythemia with 
_ Cyanosis and Enlarged Spleen; Vaquez's Disease.) 

Erythremia is a disease of the hemopoietic tissues, characterized by 
hyperactivity of the erythroblastic tissues of the bone marrow, and by 
polycythemia, chronic cyanosis, and enlarged spleen. 

Etiology. — The disease occurs with about equal frequency in the two 
sexes, and especially after the thirty-fifth year. The cause is not known. 
Some of the early cases were attributed to tuberculosis of the spleen, but 
doubt has been thrown upon the accuracy of the observation. Hyper- 
activity of the erythroblastic tissues of the bone is believed to be the 
basis of the disorder, but the initiating cause is unknown. 

Pathology. — The noteworthy changes consist of a purplish-red bone 
marrow (myelomatosis rubra) due to extraordinary hyperplasia of the 
erythroblastic tissues; and enlargement of the spleen due to hyperplasia 
of all the constituent elements, and some evidences of chronic passive 
congestion. The changes in the spleen are believed by some observers 
(Osier, etc.) to be active rather than passive; perhaps a reversion to 
the fcetal condition of erythrocytogenesis; others (Widal, Weintraud, etc. ) 
suggest that the spleen loses its function of hemolysis, in consequence of 
which erythrocytes accumulate and the erythroblastic tissues of the bone 
marrow become abnormally stimulated. The disease has been attributed 
also to diminished oxygen absorption by the erythrocytes and consequent 
hyperplasia of the erythroblastic tissues. 

" Symptoms. — The symptoms begin gradually, as a rule, in middle life 
or later; they consist of gradually increasing weakness, headache, ver- 
tigo, hebetude, and other symptoms attributable to cerebral congest ion; 
25 



386 DISEASES OF THE HEMOPOIETIC SYSTEM 

chronic cyanosis; and enlargement and fulness of the abdomen, with 
a sense of weight, especially in the region of the spleen. The skin in 
general, but especially of the face, hands, and feet, and the visible mucous 
membranes take on a peculiar, mottled, purplish-red color; the lips, ears, 
and finger tips become even darker, more dusky. The color, especially 
of the limbs, becomes darker under the influence of cold (varying thus 
with the seasons) and of gravity; and it lessens if the arms or legs be 
held upright (vasomotor instability). The cyanosis is attributable to the 
polycythemia and increased volume of blood, increased viscosity of the 
blood, slow circulation, and distended venules and capillaries (loss of 
tonicity). In long-standing cases pigmentation of the skin and mucous 
membranes ensues. Hemorrhages from the mucous membranes (nose, 
mouth, lungs, stomach, etc.) are not uncommon (stasis and impaired 
nutrition) ; occasionally they occur in the viscera, notably the brain, where 
they give rise to the ordinary phenomena and sequels of apoplexy. The 
fulness in the abdomen is due to an enlarged spleen, which is present in 
at least four-fifths of the cases. The liver also may be somewhat enlarged. 
The heart may become hypertrophied. The blood pressure is usually 
normal. Examination of the blood reveals increased (in some cases 
doubled) total volume, increased specific gravity (up to 1077), and in- 
creased viscosity (3 to 4 times the normal) ; the erythrocytes are increased 
up to 9,000,000 to 13,000,000 per cubic millimeter, the hemoglobin to 
120, 150, even 200 per cent., and the leukocytes to 10,000 or 20,000 or 
more. In a majority of the cases there is a relative increase of the 
polynuclear neutrophiles (75 to 90 per cent.), and sometimes of the large 
mononuclear leukocytes; occasionally myelocytes are seen; the erythro- 
cytes, as a rule, are normal in size, but there are some poikilocytes and 
many erythroblasts (normoblasts and megaloblasts). The blood changes 
together indicate hyperactivity of the bone marrow. 

Diagnosis. — Chronic cyanosis, enlarged spleen, and erythrocythemia 
constitute a triad of symptoms that is almost pathognomonic. One 
must eliminate other causes of chronic cyanosis, such as chronic cardiac 
and pulmonary disease, the methemoglobinemia of poisoning by coal 
tar products, so-called enterogenous cyanosis, local asphyxias (Raynaud's 
disease and allied conditions), etc. 

Prognosis. — So far as is known the disorder is ultimately fatal. It 
usually pursues a chronic course, upward of six to eight years or more. 

Treatment. — No really effective treatment is known. Removal of the 
spleen seems contra-indicated from the nature of the disease and the 
tendency to hemorrhage. Venesection is of value in relieving temporarily 
the headache, vertigo, etc. ; it may be repeated from time to time. Potas- 
sium iodide has been advocated, and oxygen by inhalation has been used 
with a view to relieve the cyanosis, but both are of at least doubtful 
utility. The arrays, as in leukemia, constitute perhaps the best treatment, 
but the data at hand are not yet sufficient to warrant a positive opinion. 



PURPURA 387 

THE HEMOERHAGIC DISEASES. 

HEMORRHAGE IN THE NEWBORN. 

Hemorrhage occasionally occurs in the newborn, and usually from 
the umbilicus, the gastro-intestinal tract, the rectum, the mouth, the 
nose, the bladder, etc. It is commonly associated with jaundice. It 
may be due to: (1) Injuries received during birth. (2) Septicopyemia 
acquired during or after birth. (3) Syphilis (syphilitic arteriocapillary 
disease), in which event it may be present even at birth, and may be 
associated with visceral hemorrhages. (4) Epidemic hemoglobinuria 
(Winckel's disease), a disorder of unknown, though probably infectious, 
nature (hospital epidemics), developing usually within the first four 
to ten days of life, and characterized by fever, jaundice, punctiform 
hemorrhages in . the tissues and organs, dyspnoea, cyanosis, gastro- 
intestinal derangements (diarrhoea), enlarged spleen, albuminuria, 
hematuria or methemoglobinuria, etc., and soon leading to death. In 
some cases there is marked fatty degeneration of the viscera (Buhl's 
disease). (5) Morbus maculosus neonatorum, a disorder clinically 
akin to morbus maculosus of the adult, and as ill understood etiologi- 
cally, although it is perhaps infectious (sometimes attended by fever, 
occurs especially in hospitals, and sometimes appears to be self-limited). 
The bleeding is perhaps most common from the bowel (melena — which 
should not be confounded with blood sucked from the breast); it may 
also occur from the stomach, mouth, nose, umbilicus, etc. Death occurs 
in 50 per cent, or more of the cases. The treatment of these disorders is 
that of syphilis or septicopyemia, to which may be added the subcu- 
taneous injection of normal human or other blood serum and such local 
measures (mentioned under hemophilia) as may tend to control the 
bleeding. 

PURPURA. 

The term purpura comprises a series of disorders characterized by 
the occurrence of hemorrhages into the skin and mucous membranes. 
Commonly, like anemia, it is symptomatic of some more or less obvious 
disorder, but often it partakes of the nature of an independent disease 
of unknown cause. One may distinguish, therefore, two types — the 
secondary or symptomatic, and the primary or idiopathic. 

The hemorrhages, so-called purpuric spots, vary in size — from small 
roundish petechias, 1 to 3 mm. or more in diameter, to larger ecchymoses, 
often irregular in outline and perhaps due to confluence of several small 
areas. Occasionally the hemorrhages are linear (vibices). When fresh 
they are bright red in color, and being extravasations they do not dis- 
appear on pressure; soon they become dark or purplish, and gradually 
transformed into reddish-brown or yellowish areas, so that at the end oi 
a week, as a rule, only more or less faintly pigmented spots remain. 



388 THE HEMORRHAGIC DISEASES 

Successive crops occasion considerable color variation of adjacent spots. 
Most frequently the legs are involved, and then in order of frequency the 
arms, the trunk, the face, and the accessible mucous membranes. 

Secondary (symptomatic) purpura occurs in: (1) Infections, such as 
typhus fever, cerebrospinal fever, and acute endocarditis — all three of 
which are especially characterized by a purpuric eruption; it may occur 
also in septicopyemia (pyococcic infections), smallpox, typhoid fever, 
scarlatina, measles, syphilis, cholera, etc. (2) Intoxications, such as 
snake bite; drug poisonings, especially with the iodides, but also bro- 
mides, quinine, salicylic acid, belladonna, copaiba, ergot, mercury, 
arsenic, etc.; and autogenic poisonings, such as may attend nephritis, 
jaundice, etc. (3) Cachectic states or nutritional disorders, such as are 
associated with the marasmus of old age (senile purpura), general 
inanition, carcinoma, sarcoma, pernicious anemia, leukemia, Hodgkin's 
disease, etc. (4) Nervous disorders (myelopathic purpura), such as 
myelitis, tabes dorsalis (in which it may follow and be confined to the 
area of the lightning pains), hysteria (hemorrhagic stigmas), neuralgias, 
such as trifacial neuralgia and sciatica (in which the purpura may be 
limited to the painful area), etc. (5) Mechanical disorders, such as 
marked venous stasis (as in heart disease, following the application of 
a tight bandage, etc.), embolism, epileptic seizures, whooping-cough 
paroxysms, local injuries, etc. Mechanical factors seem operative in 
other types of the disorder, and perhaps explain the frequency of the 
petechia? on the legs. 

Primary (idiopathic) purpura comprises several disorders, variously 
described as simple purpura, arthritic (rheumatic) purpura, hemorrhagic 
purpura, abdominal (Henoch's) purpura, etc. These differ perhaps in 
grade, intensity, or localization of the process rather than in nature. In 
the present state of our knowledge it is impossible sharply to differ- 
entiate them or satisfactorily to classify them. 

Etiology. — The disorder is most common in the second and third 
decades of life, although it occurs at all ages, and it affects males rather 
than females. The cause is not known. By some it is believed to be an 
infection or an intoxication, but neither the infectious agent nor the toxin 
has been isolated; blood cultures have usually been negative. Primary 
disturbances of the nervous system, of the liver, of the blood, and of the 
bloodvessels have been postulated. Judging from the perhaps analogous 
action of the bemorrhagin of snake venom, it seems likely that the essence 
of the process consists in an endotheliolysis of the capillaries provoked 
by some unknown poison; the primary change may occur in the blood. 

Pathology. — There are no characteristic lesions, aside from the hemor- 
rhages. In fatal cases there is high-grade anemia of the viscera with the 
usual concomitants. There may also be petechial and larger hemor- 
rhages into the serous and mucous membranes. The spleen may be 
enlarged, and there may be nephritis (usually glomerulo-nephritis). 
No constant or characteristic changes have been found in the bloodves- 
sels. During life the blood reveals the ordinary changes of secondary 



PURPURA 389 

anemia, although in some cases the erythrocytes become reduced much 
below 2,000,000 (to about 500,000 in some fatal cases); the blood platelets 
are usually remarkably reduced (20,000 or less instead of the normal 
200,000 to* 700,000). The coagulation time of the blood is usually within 
normal limits, although it may be considerably increased (delayed) ; the 
clot often is less firm than normally. 

Symptoms. — In the simplest form (so-called purpura simplex), which 
is most common in adult life, the cutaneous hemorrhages, as a rule, are 
the only noteworthy manifestation. They are usually small (petechial), 
occur in crops, and are most common on the legs and arms. Occasionally 
there is a little fever or slight pain and tenderness in the joints and 
muscles. The disorder usually lasts from two to six weeks; rarely there 
are recurring attacks that last for a year or more (chronic purpura). 

When the articular symptoms are obtrusive the disease is usually 
spoken of as purpura (or peliosus) rheumatica (or arthritica), or Schon- 
lein's disease, but it is in no way related to acute articular rheumatism. 
In about half of the cases the onset of the disease is attended with fever 
(101° to 102°), and there may be prodromal or invasion symptoms con- 
sisting of sore throat (tonsillitis), malaise, anorexia, nausea, neuromus- 
cular and articular pains and tenderness, etc. The purpuric eruption is 
like that of simple purpura, perhaps somewhat aggravated. It may be 
preceded by or associated with urticaria (purpura urticans), or erythema 
nodosum, or rarely vesiculation (pemphigoid purpura). The articular 
symptoms consist of pain, tenderness, and swelling; they are most common 
in the knees, ankles, and elbows, but may occur in other joints; they may 
antedate or occur with or subsequent to the purpura; and they usually 
last a few (four to seven) days, but may recur. 

The curious association of purpura, urticaria, erythema, angioneurotic 
oedema, and visceral lesions has been especially studied by Osier, who 
states that it occurs chiefly in children, and is characterized by relapses 
or recurrences, often extending over several years; cutaneous lesions, 
which may be simple purpura, purpura urticans, urticaria, angioneurotic 
oedema, and erythema in all its multiform varieties; gastrointestinal 
crises — pain, vomiting, and diarrhoea; joint pains or swelling, often 
trifling; hemorrhages from the mucous membranes; enlargement of the 
spleen; and nephritis (40 to 50 per cent, of the cases), which is the 
most frequent cause of death (which occurs in about 7 per cent, of the 
cases). The cases characterized by purpura or other skin lesions, gastro- 
intestinal crises, arthritis, and often nephritis, are commonly spoken of as 
Henoch's or abdominal purpura. 

In another series of cases, to the cutaneous and arthritic lesions hemor- 
rhages from the mucous membranes are added (hemorrhagic purpura, 
morbus maculosus, Werlhof). Nasal and oral hermorrhages are the 
most common; but there may be bleeding from the lungs, stomach, 
intestine, kidney, genitalia, or rarely into the retinae, brain, etc. Occa- 
sionally cases have been observed in which, for a time at least, the cutane- 
ous manifestations were absent, while the other symptoms (such as 



390 THE HEMORRHAGIC DISEASES 

visceral crises, epistaxis, etc.) seemed to justify the diagnosis (so-called 
purpura without skin lesions); in some of these cases skin lesions have 
subsequently appeared. The disease may terminate favorably within two 
weeks or thereabouts ; but death may ensue from the direct loss of blood, 
hemorrhage into the brain, etc. Occasionally in very severe cases death 
occurs within twenty-four or thirty-six hours or thereabouts (purpura 
fulminans). 

Diagnosis. — One should distinguish the symptomatic from the so- 
called idiopathic cases. The idiopathic cases may be distinguished from 
hemophilia by the absence of hereditary factors; and from scurvy by a 
knowledge of the previous history, the absence of sponginess of the gums 
(bleeding from the gums is not uncommon in purpura), the absence of 
the hemorrhagic, sclerodermic, or muscular infiltration of the thighs (so 
characteristic of scurvy), and the effect of antiscorbutic treatment. 

Prognosis. — The outlook is good except in the event of severe onset 
and rapid course (purpura fulminans), very great loss of blood, hemor- 
rhage into the brain, nephritis, and other serious complications. 

Treatment. — The treatment of symptomatic purpura is that of the 
primary or underlying disease. In the idiopathic cases rest in bed, fresh 
air, good food, iron, bitter tonics, strychnine, etc., are indicated. Good 
results sometimes attend the use of arsenic in gradually increasing doses 
to the point of toleration; and of aromatic sulphuric acid and turpentine 
(which seem to check the bleeding), and of calcium lactate (to increase 
the coagulability of the blood). Accessible bleeding spots may be treated 
as recommended in hemophilia. 



HEMOPHILIA. 

Hemophilia is a disorder, commonly hereditary, characterized by severe 
and often uncontrollable hemorrhage and lessened coagulability of the 
blood, and often associated with hemarthrosis and arthritis. 

Etiology. — Hemophilia is "the most hereditary of hereditary diseases" 
(Grandidier), and, as in the Appleton-Swain family, is known to have 
been transmitted to the seventh generation (within a period of two 
hundred years). Males usually exhibit the disorder — the proportion of 
males to females varying between 13 to 1 (Grandidier, 657 cases) and 
4 to 1 (Stempel, 209 cases); but the disease seems to be transmitted 
almost exclusively by the females. The Anglo-German races are most 
frequently attacked, but even negroes are not exempt. Hemophilic 
subjects usually are otherwise healthy; commonly they are blondes with 
soft delicate skin; often they are neurotic; usually they are remarkably 
fecund. 

The cause of the disease is not known. There is no good evidence that 
consanguinity is of etiological significance. Virchow believed in an 
abnormal tenuity and fragility of the vessels, but no noteworthy or con- 
stant changes are found. Sahli suggests an hereditary deficiency in the 



HEMOPHILIA 391 

formation of thrombokinase by the vessel wall. An infectious theory has 
been advanced, but it is not supported by any trustworthy evidence. 

Pathology. — The only constant finding in fatal cases is high-grade 
anemia and its usual consequences. In a few cases the arteries have been 
found unusually thin; in others the endothelium of the arterioles has 
proliferated; in still others the left ventricle has been hypertrophied — but 
none of these changes appears to possess any special significance. 

Symptoms. — In about three-fourths of the cases the disorder becomes 
manifest in the first two years of life (rarely in the newly born); occa- 
sionally it is delayed until the second or the third decade, rarely until 
advanced life. The characteristic of the disease is severe, often uncon- 
trollable hemorrhages, occurring spontaneously or induced by slight (or 
pronounced) trauma. The hemorrhages may be superficial — into or 
from the skin and the mucous membranes; interstitial or parenchyma- 
tous — into the subcutaneous and submucous tissues and the organs of the 
body; or they may occur into the serous sacs. The chief sources of the 
bleeding are the nose (50 per cent, of the cases), the mouth and gums (12 
per cent.), the stomach, intestines, lungs, kidneys, skin (where in con- 
trast to purpura they are rarely petechial), etc.; but they may occur from 
any part of the body, such as the urethra, vulva, uterus, tear papilla, 
eyelids, etc. The hemorrhage is usually a capillary oozing only, but it 
may be also arterial or venous, especially in the event of incised or 
lacerated wounds. The bleeding may last for hours or days, and on 
account of the large amount of blood lost may promptly lead to death; 
rarely the bleeding continues for months. The retained hemorrhages 
may give rise to smaller or larger hematomas. Minor operations, such 
as circumcision, the eruption or extraction of a tooth, vaccination, etc., 
may give rise to severe and even fatal hemorrhage; the hemorrhage of 
menstruation and of parturition may be excessive, but is usually not 
unless there are other phenomena of the disease. Joint manifestations, 
involving especially the knees and elbows, but also other joints, are 
exceedingly common; according to Konig they may be: (1) Hemarthrosis 
(pain, tenderness, swelling, perhaps fluctuation, and visible hemor- 
rhage about the joint); (2) arthritis, with fever, resembling tuberculosis; 
and (3) a condition resembling arthritis deformans. There may be 
associated muscular pains, neuralgias, etc. In some cases the tendency 
to bleeding seems to be confined to some particular part of the body 
(local hemophilia), such as the kidney (so-called renal hemophilia), 
the gastro-intestinal tract, the nose, etc., other parts of the body appar- 
ently being (temporarily or permanently) exempt. Some of the cases 
of recurring epistaxis are associated with curious multiple hereditary 
telangiectases of the nose, lips, tongues, cheek, etc. 

Following the bleedings there are the usual changes of secondary 
anemia. There may be a relative lymphocytosis. The coagulability of 
the blood is usually lessened; in some cases it has been found remark- 
ably lessened (the coagulation time being forty-five to sixty minutes or 
more); but recent studies by Sahli tend to show that the coagulability 



392 THE HEMORRHAGIC DISEASES 

may be normal or increased during the period of bleeding and lessened 
during the intervals. If the hemorrhage does not prove fatal, recovery 
is usually more rapid than after other types of bleeding. 

Diagnosis. — The familial transmission of the disease, its common 
development in early life, its usual persistence throughout life, the 
occurrence and recurrence of bleeding upon little or no provocation, the 
disproportion of the bleeding to the provoking trauma, the virtual uncon- 
trollability of the bleeding, and the joint phenomena are quite char- 
acteristic, and serve to exclude the hemorrhages of the newborn, pur- 
pura, and scurvy. 

Prognosis. — Any hemorrhage may be, but the first is rarely, fatal. Many 
if not most subjects die within the first year of life, and more than 80 per 
cent, before reaching adult life. The outlook is worse in boys than in 
girls. 

Treatment. — With a view to preventing the disease, the daughters of 
hemophiliacs should be advised not to marry — advice that is likely not to 
be heeded. The boys should avoid traumas of all sorts; they should be 
rendered as robust as possible by fresh air, good food, hydrotherapy, 
massage, tonics, etc., and operations, even minor ones, such as circum- 
cision, extraction of a tooth, etc., should be interdicted, except in the 
event of diseases otherwise threatening life. 

When hemorrhage has occurred, it may sometimes be controlled by 
rest and compression, such as plugging the nares, or the application of 
compresses to other accessible regions. Adrenalin chloride (1 to 1000), 
ice, cocaine (2 to 4 per cent.), calcium lactate or chloride (2 per cent.), 
gelatin (5 per cent, effectually sterilized), gallic acid,, tannic acid, and 
other so-called styptics may be applied locally (on the compress); but 
usually they are of little avail. Wright recommends the inhalation of 
carbon dioxide and oxygen in epistaxis. Internally calcium lactate (15 to 
20 grains, 1 to 1.3 gram, thrice daily, or 50 grains, 3.3 gram, at once) 
may be given. It is wise to intermit its administration after a few days, 
since continuous use sometimes seems to lessen, after having first in- 
creased, the coagulability of the blood. The best results appear to attend 
the use of normal blood serum (of the rabbit, horse, or man) locally, sub- 
cutaneously, and intravenously. A single injection subcutaneously of 
20 to 30 c.c. has sufficed to arrest the bleeding, but it may be necessary 
to repeat the injections daily or every two or three days until the desired 
result has been secured. In the absence of other serum, the ordinary anti- 
diphtheritic serum may be used. The arthritic lesions should be treated 
by rest (immobilization), and after several days by massage. Much 
swelling and pain may necessitate aspiration. Extreme loss of blood 
demands measures appropriate for exsanguination occurring under other 
circumstances, such as physiological saline solution intravenously, adre- 
nalin chloride, etc. (see acute secondary anemia). 



LYMPHANGITIS AND LYMPHADENITIS 393 

DISEASES OF THE LYMPH NODES AND LYMPH 

VESSELS. 

Pathological Physiology. — The lymph nodes, as has been mentioned, are 
concerned in hemopoiesis to the extent of forming perhaps most of the 
circulating lymphocytes during health; to some degree also they serve 
to protect the body against bacterial infections; they have slight phago- 
cytic properties; and they participate in the processes of hemolysis. 
The formation of lymphocytes becomes extraordinarilv augmented 
in some cases of leukemia, in which event the nodes exhibit various 
degrees of hyperplasia and metaplasia. The protection exerted against 
bacterial infection is not, as a rule, highly effective, and may become 
totally overcome, especially in severe pyococcic infections. In other 
cases, however, doubtless in consequence of chemical activities, but 
perhaps also of phagocytic properties, bacterial activity is restrained, if 
not entirely abolished; but, as is well exemplified in some cases of tuber- 
culosis, bacteria may remain for a long time latent in lymph nodes, and 
under auspicious circumstances become activated. The hemolymph 
nodes, certain nodes especially numerous in the abdomen in front of the 
vertebra?, and containing, in addition to the structures of the ordinary 
lymph nodes, sinuses filled with blood corpuscles, in general subserve 
the same functions and are subject to the same pathological conditions 
as the lymph nodes. In certain disorders, such as pernicious anemia and 
some toxic and infectious processes, they seem to be unduly concerned in 
hemolysis as well as in processes of immunity (Warthin). Whether 
these glands participate also in erythrocytogenesis has not yet been 
determined. The lymph nodes may entangle metastatic carcinomatous 
cells, and enlarging may be the first noteworthy evidence of internal 
carcinoma. 

LYMPHANGITIS AND LYMPHADENITIS. 

Lymphangitis and lymphadenitis, although they may occur separately, 
are usually associated; the process may be acute or chronic, and is 
always due to bacterial infection. The acute cases are usually due to 
the ordinary pyogenic cocci — staphylococci, streptococci, pneumococci, 
etc.; but acute lymphadenitis is common also in many of the acute 
specific infectious diseases, such as diphtheria, scarlatina, measles, 
chickenpox, erysipelas, plague, glandular fever, typhoid fever, gonor- 
rhoea, chancroid, as well as rickets, lymphatic constitution, etc.; the 
chronic cases are due usually to tuberculosis or syphilis. The infection 
in lymphangitis is usually acquired by means of a wound, but this is not 
always necessary, since infection seems sometimes to be acquired without 
or with only the slightest abrasion, as at necropsies, operations on sep- 
ticopyemic patients, etc. The infectious agent may enter the lymph vessel 



394 DISEASES OF THE LYMPH NODES AND LYMPH VESSELS 

directly from the wound, or it may invade the vessel wall from without. 
In lymphadenitis the infection may be lymphogenous, in which event it is 
likely to be localized; or it may be hematogenous, in which event it is 
likely to be generalized (as in some of the specific infectious diseases). 

Pathology. — Acute lymphangitis is commonly a part of pyococcic 
infection (septicopyemia) and partakes of the nature of such infections. 
It may involve only circumscribed areas (reticular lymphangitis), or the 
lymphatic trunks (tubular lymphangitis). The endothelial cells lining 
the lymph spaces swell and later desquamate, and together with leuko- 
cytes, serum, and fibrin obstruct the vessel. This inflammatory exudate 
commonly coagulates and the vessel becomes completely thrombosed 
and surrounded by more or less inflammatory congestion and oedema 
(perilymphangitis); occasionally small foci of hemorrhage supervene. 
Resolution, suppuration, or organization may ensue, depending upon 
the virulence of the infecting agent and the resistance of the individual. 
In the event of suppuration, phlegmonous infiltration may follow. In 
the event of organization, proliferation and thickening of the vessel wall 
and complete obstruction of the lumen usually supervene. 

In most cases the lymph nodes participate in the process and local or 
general lymphadenitis results. The local process is well seen in infections 
of the hands and arms (axillary nodes) or of the feet and legs (femoral 
nodes); in infections of the mouth, carious teeth, facial erysipelas, ton- 
sillitis, etc. (cervical nodes); in pneumonia, bronchitis, especially in chil- 
dren, tuberculosis, etc. (bronchial nodes); in appendicitis, typhoid fever 
(mesenteric and retroperitoneal nodes); in gonorrhoea and chancroid 
(inguinal nodes, so-called bubo) ; etc. The general process is common in 
the aforementioned infectious diseases, but occurs notably in glandular 
fever, tuberculosis, syphilis, plague, etc. In the acute cases the nodes 
become enlarged, swollen, soft, and hyperemic; resolution may occur, or 
liquefaction, necrosis, and suppuration may ensue. Microscopically there 
is lymphoid hyperplasia, vascular dilatation, polynuclear leukocytic infil- 
tration, fibrin formation, and swelling and desquamation of the endo- 
thelium of the sinuses. Considerable necroses may occur, as in typhoid 
fever; or the process may become hemorrhagic or purulent. In the 
chronic cases there is a low-grade, chronic, inflammatory process, with 
the formation of cicatricial connective tissue, in consequence of which 
the nodes become firm, hard, and small; the capsule becomes thickened, 
the sinuses more or less obliterated or obstructed, and the lymphoid 
tissue atrophic. 

Symptoms. — Reticular lymphangitis manifests itself by circumscribed, 
red, swollen, painful, and tender areas, which are commonly seen on the 
arms or legs, and progress usually from the periphery toward the centre; 
frequently there is considerable collateral oedema. Tubular lymph- 
angitis manifests itself in cord-like, irregular, reddish streaks beneath 
the skin, progressing from the periphery toward the regional glands. 
As already stated, both varieties are commonly associated, and there 
is usually concurrent inflammation of the regional lymph nodes — 



LYMPH ANGIECTAS1S 395 

which become swollen, painful, and tender. The general symptoms are 
those of pyococcic infection — malaise, chilliness, and fever, in degree 
depending upon the severity of the infection. In the event of suppura- 
tion, the common symptoms of septicopyemia (chills, fever, sweats, and 
leukocytosis) supervene, and if the lymph nodes are involved they become 
softened and fluctuating, and may rupture. In the event of chronic 
proliferation the lymph vessels become thickened, cord-like, and chronic 
oedema due to obstruction occurs, unless a collateral circulation develops. 
If a large trunk is involved a considerable area of the body may become 
chronically cedematous or elephantiatic, or chyluria or lymphorrhagia, 
etc., may ensue. 

Involvement of the deep intrathoracic and intra-abdominal lymph 
vessels and nodes may be difficult or impossible of diagnosis, since, 
aside from local pain and perhaps tenderness, symptoms may be absent 
or in abeyance. The considerable enlargement of the bronchial nodes 
that sometimes occurs in children is suggested by dyspnoea, respiratory 
stridor, sometimes dysphagia, and the physical signs of bronchial stenosis 
(dulness over the vertebrae, x-ra,y examination, etc.). Sudden death 
occasionally ensues from suppuration and rupture into the trachea or a 
bronchus. 

The general lymphadenitis of the acute specific infections is manifested 
by swollen, painful, and tender nodes occurring during the course of 
these infections. In the chronic cases, there may be only enlargement 
of the lymph nodes; sometimes they are more or less tender, and they 
may become quite hard. 

Diagnosis. — In the acute cases phlebitis usually may be excluded 
by the fact that in lymphangitis the redness is more marked and more 
superficial and follows the lymph vessels (rather than a vein), and the 
deep-seated cord-like induration in phlebitis or a thrombosed vein is 
absent; in addition the neighboring lymph nodes are usually involved. In 
the chronic cases one must differentiate between the divers sorts of 
glandular enlargement (see tumors and tumor-like formations) . Some- 
times it may be necessary to excise one of the enlarged lymph nodes in 
order to come to a definite conclusion. 

Prognosis. — The prognosis depends entirely upon the nature and 
severity of the infection and the resistance of the patient. 

Treatment. — In the acute cases the treatment is that of the primary 
pyococcic infection together with rest to the affected part, the local 
applications mentioned in connection with erysipelas, etc. Surgical 
measures eventually may be necessary. 



LYMPHANGIECTASIS. 

(Elephantiasis.) 

Lymphangiectasis, dilatation of the lymph vessels, may be congenital 
or acquired. The congenital variety results from mechanical or in flam- 



396 DISEASES OF THE LYMPH NODES AND LYMPH VESSELS 

matory obstruction of the lymph vessels occurring during intra-uterine 
life; but some cases developing in adult life without an obvious cause 
seem perhaps referable to a congenital or inherited predisposition. The 
acquired variety may be: (1) Parasitic, due to obstruction of the vessels 
by Filaria bancrofti — the different forms of tropical and subtropi- 
cal elephantiasis, chylous ascites, chyluria, etc., the result of obstruc- 
tion of the thoracic duct, etc.; and (2) non-parasitic, which occasion- 
ally results from inflammation and thrombosis of the lymph vessels 
(erysipelas, eczema, infected leg ulcers, etc.); or it may be secondary 
to cicatricial occlusion of the vessels, to the pressure of tumors, to the 
blocking of the lumen by tuberculous or carcinomatous material, to the 
extirpation of lymph nodes, etc. The condition, however, is rare, 
despite the frequent operation of the causative factors, since such is the 
free communication between the lymphatics that a collateral circulation 
is readily established. 

Symptoms. — The dilated vessels, noticeable only when situated super- 
ficially, that is, in the skin (and due then to obstruction of the deeper 
lymphatics), appear as soft, transparent sacs or vesicles, often arranged 
in clusters, and filled with clear or milky lymph. These, which are 
sometimes spoken of as circumscribed lymphangiomas, are found most 
commonly in regions rich in superficial lymph plexuses, especially along 
the inner aspect of the thigh, about the genitalia, on the anterior abdom- 
inal wall, in the mesentery (chyle or lymph cysts), etc. Rupture of the 
vesicles is not infrequent, and sometimes results in the escape of con- 
siderable lymph (lymphorrhagia, chylous ascites, etc.). In some cases 
the obstruction produces diffuse or widespread dilatation of the lymph 
vessels — usually of the leg or the external genitalia (elephantiasis, lymph 
scrotum, lymph vulva), although it may occur anywhere. The limb 
(or other portion of the body) becomes greatly swollen, hard, indurated, 
and non-reducible— a condition of branny induration, due to hyperplasia 
and connective-tissue overgrowth of the lymph vessels, skin, and sub- 
cutaneous tissues, and chronic oedema from obstruction of the lymph 
vessels. The limb may be soft and doughy (elephantiasis mollis), or 
quite hard (elephantiasis dura); and the overlying skin may be thin, 
smooth, and translucent, or quite thick and horny (pachydermia). 
Ulceration may supervene, and permit of the escape of more or less 
lymph — a turbid, milky-white fluid. 

Prognosis. — The outlook is not especially hopeful: the condition is 
usually permanent. 

Treatment. — In the circumscribed form relief may sometimes, but 
rarely, be obtained by extirpation of the dilated vessels; but when the 
condition is diffuse, temporary relief only may be afforded by massage, 
an elastic bandage, and elevation of the limb — in the hope that a suffi- 
cient collateral circulation ultimately may be established. 



TUMORS AND TUMOR-LIKE FORMATIONS 397 



TUMORS AND TUMOR-LIKE FORMATIONS. 

The lymph vessels are not infrequently the seat of tumor formations, 
of which, two types may be distinguished — lymphangioma and endo- 
thelioma (lymphangiosarcoma). The lymphangioma, which ordinarily 
is classed as a benign tumor, consists of multiplied and dilated lymph 
spaces (telangiectatic or cavernous) lined with endothelium and con- 
taining lymph. They are most common in the skin and subcutaneous 
tissues, but they occur also in the internal organs, the mesentery, etc. 
Common examples are the small plexiform lymphangiomas of the skin, 
macroglossia, macrocheilia, and certain cystic tumors of the neck, 
mesentery, etc. The endothelioma is a tumor developed from the 
endothelium of lymphatic spaces, and is found most commonly in the 
serous membranes, the salivary glands, the skin, the ovary, the testicle, 
etc. In addition, the lymph vessels serve as the common source of the 
local and distant spread of carcinoma, rarely also of sarcoma. 

The lymph nodes also are the seat of a number of tumors and tumor- 
like growths, which have been variously described as lymphoma, 
lymphadenoma, lymphocytoma, lymphosarcoma, malignant lymphoma, 
leukosarcoma, lymphomatosis, adenie, pseudoleukemia, Hodgkin's 
disease, etc. Not only is there much confusion in regard to the identity 
of the disease or diseases comprised in these terms, but also in regard to 
their relation or supposed relation to leukemia, on the one hand, and 
to syphilis and tuberculosis of the lymph nodes, on the other hand. In 
the majority of cases, however, one can separate with tolerable ease and 
certainty the lymphatic enlargements due to syphilis or tuberculosis; 
and ordinarily the enlargements due to leukemia present no diagnostic 
difficulties. Most of the other lymphatic enlargements seem to be more 
or less related clinically and pathologically; studying them generally, 
they seem to exhibit gradations and stages of transition. Thus, there 
is undoubtedly a leukemic and an aleukemic lymphoma; that is, a dis- 
order characterized by enlarged lymph nodes with or without the leukemic 
blood picture; the one disease is leukemia in a true sense, the other may 
be spoken of as pseudoleukemia or Hodgkin's disease. Differentiation 
is rendered difficult by the fact that, as pointed out by Reed, Longcope, 
and Warthin, Hodgkin's disease seems to have a characteristic histo- 
logical picture; that the other cases, of which the histological charac- 
teristic is hyperplasia of lymphoid tissue, sometimes do and sometimes 
do not exhibit the leukemic blood picture, that is, aleukemic lymphomas 
sometimes progress to true leukemia (perhaps early and late stages oi 
the one disease); and that true leukemia, during the not unknown periods 
of regression (occurring spontaneously, or induced by treatment), may 
exhibit the blood picture of aleukemic lymphoma (sometimes, however, 
the blood is qualitatively if not quantitatively leukemic). Furthermore, 
there are transition stages between some of these cases, especially the 
aleukemic lymphomas, which sometimes are spoken of as benign lymph- 



398 DISEASES OF THE LYMPH NODES AND LYMPH VESSELS 

omas, and so-called malignant lymphomas; that is, there is no sharp 
line of demarcation between the cases of lymphoid hyperplasia that do 
not and those that do infiltrate and ultimately penetrate the capsules of 
the lymph nodes and invade the adjacent tissues. The difference be- 
tween the benign and the malignant lymphoma (lymphosarcoma) seems 
to be one of degree only. On the other hand, the ordinary varieties 
of sarcoma (round-cell, spindle-cell, angiosarcoma, etc.) may implicate 
the lymph nodes; they differ from the lymphomas (lymphoid hyperplasias) 
in that, as do sarcomas generally, they give rise to hematogenous metas- 
tases, and that, as a rule, they do not progressively involve adjacent sets 
of lymph nodes (as do the lymphomas). 

In the present state of our knowledge we may differentiate the follow- 
ing varieties of chronic progressive enlargement of the lymph nodes: 

(1) Those due to specific infections, such as tuberculosis and syphilis; 

(2) those due to leukemia, of which there may be a preleukemic, an aleu- 
kemic, or a subleukemic stage; (3) tumor formations (lymphomas), 
among which one may include lymphosarcoma (malignant lymphoma), 
the ordinary types of sarcoma (round-cell, spindle-cell, angiosarcoma, 
etc.), as well as secondary or metastatic carcinomatous growths; and 
(4) Hodgkin's disease. The specific infections and leukemia have 
already been discussed; some of the cases included under (3) the lymph- 
omas, may be an early stage or a forme fruste of, or progress to, leukemia; 
clinically, it is usually impossible to distinguish between the so-called 
lymphomas and Hodgkin's disease, except by microscopic examination 
of an excised lymph node. 



HODGKIN'S DISEASE. 

Hodgkin's disease is a disorder of the lymph nodes characterized 
anatomically by a peculiar, chronic, perhaps inflammatory process 
leading to well-marked fibrosis, and clinically by enlargement of the 
lymph nodes, progressive anemia, and a fatal termination. 

Etiology. — Hodgkin's disease is twice or thrice as common in men as 
in women, and although it may occur at any age, it is especially common 
in young adults (fifteenth to thirty-fifth year). The cause of the disease 
is not known. A number of cases have been attributed to tuberculosis, 
but there is no doubt that although tuberculosis of the lymph nodes 
may follow an aberrant clinical and pathological course, the great 
majority, if not all cases, can be readily distinguished from Hodgkin's 
disease. 

Pathology. — The lesions consist of progressive enlargement of the 
lymph nodes, which usually involves first the cervical nodes, and then in 
order of frequency the axillary, the inguinal, the thoracic, and the 
abdominal nodes. In some cases the disorder seems to begin in the 
deeper nodes, the superficial nodes being involved later; in other cases 
the enlargement is for a long time circumscribed to one set of nodes, later 



HODGKIN'S DISEASE 399 

perhaps but sometimes not becoming generalized. The lymph nodes 
vary much in size; they are smooth and spheroidal in shape, soft, and 
inelastic (sometimes even fluctuating), or firm and discrete, even the 
largest masses in many cases being made up of discrete nodules bound 
together by connective tissue. Occasionally, however, adjacent nodules 
fuse through penetration of the capsules, and they may become adherent 
to the overlying subcutaneous tissues and skin. On section the nodules 
are pinkish and semitranslucent, or grayish or yellowish, especially 
if softening and fibrosis have occurred. The microscopic appearances, 
which are characteristic, consist at first of hyperplasia of the lymphoid 
cells, especially of the germinal centres, with proliferation of the endo- 
thelial and reticular cells — a process that much resembles chronic in- 
flammation. The cellular proliferation and thickening of the reticulum 
soon obscure the normal structures, so that only indefinite remains 
of the lymphoid tissue can be identified. In addition to lymphocytes, 
polynuclear leukocytes, plasma cells, and endothelioid cells, eosinophiles 
and mononuclear and multinuclear giant cells are found in consider- 
able numbers, and are considered quite characteristic (Reed, Longcope, 
Warthin). Ultimately the fibrosis becomes extreme, so that the nodes 
become converted almost completely into fibrous tissue. Nodules of 
similar formation are sometimes found in the spleen (which may become 
considerably enlarged), in the liver, gastro-intestinal tract, kidneys, lungs, 
bronchi, thymus, bone marrow, serous surfaces, skin, etc.; these are most 
likely not true metastases, but (as in leukemia) hyperplasias of previously 
existing areas of lymphoid tissues. 

Symptoms. — The first symptoms, as a rule, consist of painless enlarge- 
ment of the lymph nodes, which, as a rule, begins in one side of the 
neck, although it may begin elsewhere; in most cases the cervical, axillary, 
inguinal, thoracic, and abdominal nodes become progressively involved, 
in some cases soon, in some cases later; rarely the disease remains local- 
ized to the set of nodes first involved. The local mass of enlarged 
nodes often becomes very large, but, as a rule, the individual nodes can 
be distinctly palpated, although rarely they fuse and perhaps form 
adhesions with the superjacent subcutaneous tissues and the skin. The 
nodes may be soft (sometimes fluctuating) or firm; sometimes, in ad- 
vanced cases, quite hard. Divers symptoms result from local pressure: 
oedema and cyanosis of the neck, face, arm, or leg; effusions within the 
serous cavities; dyspnoea, generalized cyanosis, dysphagia, and other 
manifestations of mediastinal tumor; jaundice, pyloric obstruction, 
and other gastro-intestinal disturbances; sciatica and other local pains, 
etc. In some cases the deep (thoracic and abdominal) nodes are firsl 
involved, so that these usually late symptoms of pressure may be the 
earliest manifestations. The spleen is commonly enlarged, sometimes 
notably enlarged; the liver also is enlarged in about one-half the cases. 
The skin may become pigmented (independently of the use of arsenic); 
pruritus and furuncles are often annoying; lymphomatous nodules 



400 DISEASES OF THE LYMPH NODES AND LYMPH VESSELS 

sometimes occur in the skin, and subcutaneous hemorrhages occasion- 
ally have been observed. 

In the ordinary, slowly progressing cases, the general health, aside 
from more or less malaise, usually remains for a long time unimpaired. 
In some cases there is more or less fever: it may be a mild continued 
fever (as high as 100° or 101°); or especially toward the end it may be 
high (104° to 105°) with daily remission of three or four degrees and 
accompanied with chills and sweats; or it may be of the relapsing type 
(Epstein-Pel) — periods of fever of ten to fourteen days' duration alter- 
nating with periods of apyrexia. Secondary anemia, ultimately of high 
grade (2,000,000 erythrocytes or less, 30 to 40 per cent, of hemoglobin), 
emaciation, and cachexia gradually develop — sometimes soon and pro- 
gress rapidly; or the disorder previously quiescent suddenly becomes active 
and soon leads to death. The leukocytes reveal no characteristic changes ; 
occasionally there is a slight leukocytosis (10,000 to 20,000), but rarely any 
relative lymphocytosis; occasionally an eosinophilia has been observed. 

Diagnosis. — Clinically the disease is often not an entity sharply 
distinguishable from other forms of glandular enlargement. The 
diagnosis virtually depends upon painless, discrete, progressive enlarge- 
ment of the lymph nodes unassociated with leukemic changes in the 
blood ; but in the differential diagnosis one must remember that leukemia 
may have a preleukemic, an aleukemic, and a subleukemic stage. 
Excision and microscopic examination of an enlarged gland may be the 
only way to a correct diagnosis in some cases. Some cases of sarcoma 
(round-cell, spindle-cell, lymphosarcoma) of the lymph nodes often 
resemble Hodgkin's disease, but, as a rule, in sarcoma growth is rapid 
and often painful, infiltration and penetration of the capsules of the nodes, 
fusion of the nodes, and infiltration of the adjacent tissues occur early, 
metastases are common, and the primary as well as secondary growths 
may soften, ulcerate, and discharge externally. Sarcoma, however, 
may be painless and the enlarged nodes of Hodgkin's disease may not 
remain discrete, so that a differential diagnosis may not be possible in 
the absence of a microscopic examination of an excised node. Tuber- 
culosis of the lymph nodes rather than Hodgkin's disease is suggested 
by a tuberculous focus elsewhere in the body, the tendency of the en- 
larged nodes to fuse, form adhesions with the skin, soften, suppurate, 
and discharge, and a response to the tuberculin tests ; but a microscopic 
examination of a node or bacteriological examination of the purulent 
discharge may be necessary to establish the diagnosis. Syphilis may 
be distinguished by the history and concomitant evidences of syphilis 
elsewhere in the body. The types of splenomegaly formerly called 
splenic pseudoleukemia, von Jaksch's disease, etc., and the tumor for- 
mation known as multiple myeloma, and formerly called medullary 
or myelogenous pseudoleukemia, are in no way related to Hodgkin's 
disease. Multiple myeloma (occurring especially in the ends of the long- 
bones, the ribs, the vertebrae, etc.) is characterized by deep-seated, 
sometimes pulsatile (bone) pains, bony enlargements, perhaps spon- 



DISEASES OF THE THORACIC DUCT 401 

taneous fractures, divers motor and sensory phenomena due to the 
local growths, fever, anemia without leukocytosis (perhaps occasion- 
ally relative lymphocytosis), and Bence- Jones albumosuria (so-called 
myelopathic albumosuria, Kahler's disease). 

Prognosis. — The disease is invariably fatal. Most subjects rarely 
live more than three years; very mild and slowly progressive cases may 
continue six years or more. Periods of quiescence, with spontaneous 
regression of the enlarged lymph nodes, apyrexia, and improvement in 
the general health sometimes occur, and may last for months; or the dis- 
ease for some time mild and non-progressive suddenly takes on malignant 
characteristics and speedily leads to death. Death may result from pro- 
gressive anemia, cachexia, and asthenia; or from tuberculosis or other 
secondary infection (sometimes answerable for the high fever toward 
the end). 

Treatment. — The nature of the disease makes it especially refractory 
to treatment. The best results (lessening of the progress of the disease) 
have been attained by the use of arsenic and the x-ysljs, which should 
be employed as advised in leukemia. Operative removal of all the 
regional lymph nodes in the localized form of the disease has rarely been 
of some temporary avail, but, as a rule, all nodes cannot be removed, 
and those left soon take on renewed growth. 



DISEASES OF THE THORACIC DUCT. 

The thoracic duct is formed by the confluence of the main trunk or 
trunks of the intestinal lymphatics and the main lumbar trunks which 
have resulted from the union of the lymphatics of the pelvis, genitalia, 
abdominal wall, and lower extremities. The point of union is on a level 
with the first or second lumbar vertebra, and is usually indicated by a 
saccular dilatation — the receptaculum chyli. Thence the thoracic duct 
courses through the posterior mediastinum, and, being joined by the 
main trunk of the lymphatics of the upper part of the body (except those 
of the right side of the head and thorax), eventually empties into the left 
subclavian vein distal to its union with the internal jugular. The right 
thoracic (or lymphatic) duct empties into the right subclavian (some- 
times internal jugular) vein. Anatomical anomalies, however, are by no 
means rare. 

Pathology. — The thoracic duct is subject to divers disorders of con- 
siderable interest in clinical medicine: (1) It is a common source of the 
rapid dissemination of tubercle bacilli throughout the body— by way 
of the lymph and blood streams. The duct often acts merely as a 
passive carrier of bacilli discharged by a tuberculous lymph node some- 
where within the area of collection of its tributaries; sometimes if is 
itself tuberculous. There is considerable evidence also that it is the 
avenue of general distribution of pyococci in many cases of septico- 
pyemia; and of carcinomatosis developing primarily in the abdomen 
26 



402 DISEASES OF THE THYMUS BODY 

or pelvis. (2) It is often the seat of different disorders, of which the 
ultimate consequence is obstruction. This may arise from thrombi, 
parasites (Filaria bancrofti), secondary tumor masses, etc., within the 
duct; acute and chronic inflammation or primary tumor formation 
of the duct itself; compression of the duct from without by regional 
inflammatory exudates, cicatrices, enlarged lymph nodes, tumors, aneu- 
rysm, etc.; or thrombosis of the subclavian vein. The consequences 
vary with the site and degree of the obstruction. If the obstruction is 
incomplete, an efficient collateral circulation may become established 
and there may be no noteworthy symptoms ; this may ensue also when the 
obstruction is low down. When the obstruction is complete and high up, 
the duct usually becomes dilated; the receptaculum chyli may become 
as large as a walnut or a hen's egg (perhaps apparent on palpation of the 
abdomen). Sometimes the dilatation extends to the peritoneal tributaries 
of the duct, giving rise to lymph or chyle cysts (so-called chyle angiomas, 
which, however, often have a local inflammatory peritoneal cause, or 
resemble tumor formations). In some cases of extreme obstruction 
rupture of the duct ensues. 

Symptoms. — The symptoms are those of stasis of chyle, with the 
eventual development, in consequence of transudation of the chyle or 
rupture of the vessels, of chyloperitoneum (chylous, milky, opalescent 
ascites), and chylothorax; perhaps also chylopericardium, chyluria, and 
chylous swelling of the abdominal wall, external genitalia, legs, etc. 
In the event of rupture of the duct rapid emaciation usually ensues. 

Diagnosis. — It is sometimes difficult to distinguish chylous from so-called 
chyliform fluid which (in the absence of obstruction of the lymphatics) 
sometimes develops in the peritoneum, pleura, etc.; it is due to fatty 
metamorphosis of leukocytes (pus cells), endothelium, and tumor cells, 
and has been found in chronic, especially tuberculous, inflammations of 
the serous membranes, endothelioma, chronic heart disease, cirrhosis of 
the liver, etc. The presence of fine (rather than coarse) fatty droplets 
and of sugar suggests, but is not conclusive evidence of, the chylous origin 
of the fluid; in some cases of chyliform fluid the origin of the fat is evident 
in the presence of fatty degenerated cells. 

Prognosis. — The prognosis is bad, as a rule; but it depends upon the 
nature and completeness of the obstruction. Occasionally an efficient 
collateral circulation becomes established, or a thrombus, for instance, 
may become softened and permit of some circulation through the duct, 
or the course of the obstruction being removable, may be removed. 

Treatment. — The treatment, in cases in which any treatment is of 
avail, is purely surgical. 

DISEASES OF THE THYMUS BODY. 

Pathological Physiology. — The thymus body ordinarily attains its 
greatest development at the end of the second year of life. Thereafter 
it gradually atrophies until puberty, whereupon the atrophic process 



ENLARGEMENT OF THE THYMUS . 403 

becomes more rapid, so that in adult life the body is represented by a 
small mass of fibro-adipose tissue containing Hassell's corpuscles (rem- 
nants of the original epithelial tissue) and a small amount of lymphoid 
tissue. Anatomically and functionally the thymus is to be classified with 
the lymphoid tissues, especially since nothing is known of the function 
of Hassell's corpuscles, and there is no certain evidence that the thymus 
produces a specific internal secretion. There is some evidence, however, 
that an obscure and ill-comprehended relationship exists between the 
thymus and organs that do produce an internal secretion, such as the 
thyroid (in Graves' disease), parathyroids, pituitary body (in akromegaly), 
the ovaries, testicles (atrophying as the sexual organs develop), etc.; 
and extracts of the thymus are said to cause a fall in blood pressure and 
rapid action of the heart. Like adenoid tissue generally, the thymus is 
the seat of lymphocyte formation, especially in early life when thev are 
produced in abundance; furthermore, upon slender basis, the thymus is 
said to exert some influence upon the growth of the bone and the develop- 
ment of the cerebral functions, and to participate in the processes of 
immunity. The thymus persists in castrated animals. Apparently the 
thymus is rarely the seat of primary disease, the only known disorder of 
clinical significance being enlargement or hypertrophy, in some way 
concerned in thymic asthma and thymic death. 

Enlargement is sometimes found also in leukemia, Hodgkin's disease, 
rachitis, Graves' disease, Addison's disease, akromegaly, myasthenia 
gravis, etc., as well as in tumor formations (primary, that is, benign and 
malignant lymphoma, and secondary), cyst formations, etc. The thymus 
may be affected secondarily also in a number of disorders, such as acute 
especially pyococcic infection (acute simple, or suppurative thymitis), 
chronic infections (tuberculosis, syphilis, etc.). Rarely, pathological 
atrophy has been encountered in some cases of infantile marasmus, 
but it is probably part of the general process rather than of etiological 
significance. Extracts (fresh or dried) of the thymus have been used 
with varying success in arthritis deformans, rickets, myxoedema, Graves 1 
disease, Addison's disease, etc. 



ENLARGEMENT OF THE THYMUS. 

(Hypertrophy, Hyperplasia, Persistence of the Thymus; Status Lymphaticus; 
Lymphatism; Thymic Asthma; Thymic Death; Thymic Tracheostenosis.) 

Aside from the disorders already mentioned in which the thymus 
may be enlarged, enlargement is found in a series of cases characterized 
by stridorous dyspnoea, asthma, or sudden death. Some authors main- 
tain '(although others deny) that the thymic enlargement is the cause of 
the stridor, asthma, and death which it is believed to provoke by pressure 
on the trachea (tracheal stenosis), on the vagus, or other of the medi- 
astinal tissues or organs. 

The enlargement is a hyperplasia of unknown cause; it has been 



404 DISEASES OF THE THYMUS BODY 

referred to divers sorts of infections, intoxications, and disorders of meta- 
bolism. Often it is associated with adenoids, enlarged tonsils, enlarged 
lymph nodes generally, enlarged spleen, and reddish bone marrow (status 
lymphaticus) ; sometimes also there is hypoplasia of the heart and 
aorta, infantilism, etc. There has been much discussion as to whether 
enlargement of the thymus can cause tracheal stenosis. Warthin, who 
has studied the subject attentively, maintains that it may; suggesting the 
use of the term " thymic tracheostenosis, " he states that "all the symp- 
toms and all the operative and postmortem evidence point to a suffo- 
cation resulting from tracheal stenosis. Secondary laryngeal spasm 
is the chief if not the only cause of the fatal termination. To these 
may be added other effects of compression upon the heart, great vessels, 
vagi, and recurrent nerves. To a reflex spasm of the glottis may be added 
a reflex cardiac paralysis, as the latter may alone be the direct cause of 
death in those cases of sudden death in which all signs of tracheal stenosis 
or laryngeal stenosis are wanting." "Status lymphaticus may be the 
consequence of a number of primary morbid processes, such as syphilis, 
rachitis, some latent infection, auto-intoxication, etc., that are character- 
ized by excessive demands upon the lymphoid and myeloid tissues. The 
sudden death is dependent primarily and wholly upon the thymic enlarge- 
ment, and the latter condition becomes, therefore, the most important 
feature clinically." Other observers believe that there is a toxic ele- 
ment in the condition. 

Symptoms. — The symptoms are said by Warthin to consist of respira- 
tory disturbances resulting from the diminution of space in the superior 
thoracic strait. He distinguishes three classes of cases according to their 
severity — thymic stridor, thymic asthma, and thymic death. The stridor 
is usually congenital or develops soon after birth; it is inspiratory and 
expiratory; it may be stationary or progressive, or it may manifest 
itself suddenly in its most marked form; it may be precipitated by a fit 
of screaming or crying, or it may come on during one of the acute infec- 
tions. It varies much in intensity; it is unassociated with changes in the 
voice, and persists during sleep, although it lessens in severity. Thy- 
mic asthma (Kopp's asthma, Millar's asthma) is an exacerbation of 
stridor of asthmatic character, or it may develop in a child showing no 
previous sign of stridor. The first attack may be fatal, or there may be 
periodical recurrences of progressive character; but an attack may sub- 
side quickly. There is no sharp line of demarcation between thymic 
asthma and thymic death, but the term thymic death has come to be 
applied to those cases in which death occurs suddenly without definite 
history of previous respiratory difficulty. It may be induced by divers 
causes, such as anesthesia, slight surgical operations, fright, etc. The 
general picture is that of a convulsive attack of thymic asthma of 
severest type ending in death (Warthin). 

Physical examination discloses an area of dulness at the upper part 
of and somewhat to both sides of the sternum, merging with the upper 
limit of the cardiac dulness. Sometimes there is distinct bulging, or a 



DISEASES OF THE SPLEEN 405 

palpable swelling in the episternal notch. A shadow may be disclosed 
by the cc-rays. Tracheal or bronchial stenosis may be seen by the 
bronchoscope or after tracheotomy. The child may be rachitic or 
anemic. Examination of the blood may reveal a relative lymphocytosis. 

Diagnosis. — A congenital chronic stridor both inspiratory and expira- 
tory, but most marked on inspiration, with a tendency to exacerbations, 
and the production of dyspnoea so marked as to occasion intubation 
and tracheotomy, and finally death, is usually due to thymic enlargement 
(Warthin). 

Prognosis. — The prognosis is bad. 

Treatment. — The underlying rickets, anemia, or malnutrition, should 
be treated, so as to prevent, if possible, the onset of symptoms referable 
to the enlarged thymus. By avoiding excitement, operations, etc., attacks 
may be prevented. During the attack the child should be kept hori- 
zontal, at least the head forward, cold applications should be applied 
to the chest or the child should be immersed in a full warm bath, and 
supportive measures should be used. Intubation with a long tube 
through the mouth, or through a tracheotomy wound, may be resorted to. 
The arrays may be of service, as in leukemic conditions, but until more 
data are accumulated they must be employed with caution . The thymus 
has been removed in several cases with good results. 



DISEASES OF THE SPLEEN. 

Pathological Physiology. — The functions of the spleen are ill under- 
stood. The organ seems to be non-essential to life, and it apparently 
does not produce an internal secretion — whence it cannot be classed with 
the ductless glands. In general it may be said functionally and ana- 
tomically to resemble the lymph nodes — which take on a compensatory 
hyperplasia after splenectomy. During foetal life the spleen is the seat 
of erythrocytogenesis, a function to which apparently it may revert in 
the stress of circumstances in later life. In diseases of the hemopoietic 
system, especially leukemia, as already mentioned, it undergoes consider- 
able hyperplasia or metaplasia, so that, especially in myelocytic leukemia, 
it may become converted into a tissue much resembling, almost identical 
with, the bone marrow. It seems to be actively concerned in hemolysis : 
perhaps during health its action in this regard is rather passive, the 
organ acting merely as a scavenger, or as a graveyard for blood corpuscles 
incapacitated or destroyed elsewhere in the economy; in diseased condi- 
tions, however, hemolysis seems to be active in the spleen, and, as in 
pernicious anemia, this may be a contributory factor in the fatal termina- 
tion. The spleen also is concerned in the processes of immunity; this is 
obvious in the splenic phagocytosis, but perhaps the organ exerts also a 
chemical non-phagocytic immunizing influence. 



406 DISEASES OF THE SPLEEN 



ANOMALIES OF FORM AND POSITION OF THE SPLEEN. 

In association usually with other errors of development, the spleen 
may be absent, abnormally small, abnormally large, or misplaced in 
the abdominal or thoracic cavity; it is sometimes unusually lobulated; 
and small supernumerary or accessory spleens are quite common. Clini- 
cal interest attaches to the presence of the spleen in the right side in 
transposition of the viscera. 

Movable spleen (floating spleen, splenoptosis). Rarely, and then only 
in the event of considerable enlargement, the spleen may be unduly 
movable without evidences of displacement of the other abdominal 
organs; but usually splenoptosis is merely part of general visceroptosis. 



RUPTURE OF THE SPLEEN. 

Rupture of the spleen may occur spontaneously or in consequence of 
trauma. Severe trauma may cause rupture of a previously normal 
spleen; but commonly rupture results from slight trauma, although it 
may occur spontaneously, in a spleen already diseased, such as the 
acute enlargements of typhoid, relapsing, or malarial fever (especially 
in .the tropics), infarct and abscess, etc. The trauma may consist of 
coughing, rough handling, as in palpation, puncture by an exploring 
needle, etc. The symptoms consist of local pain and distress, and 
the shock and other phenomena attending intraperitoneal hemorrhage. 
The treatment is surgical, and should be instituted immediately. 



THROMBOSIS, EMBOLISM, AND ABSCESS OF THE SPLEEN. 

Thrombosis of the splenic vein rarely develops in the course of typhoid 
fever or local inflammatory disorders (such as of the pancreas, etc.); it may 
result from extension of a thrombus in the portal or mesenteric veins, or 
follow sclerosis and atheroma of the splenic vein. The symptoms consist 
in the main of venous engorgement, enlargement and perhaps infarction 
of the spleen, recurring hematemesis, and other manifestations suggest- 
ing splenic anemia, although it differs in the more common, acute onset. 
Embolism develops usually in the course of acute or chronic valvular 
disease of the heart and septicopyemic processes ; it may follow primary 
splenic arterial or venous thrombosis. The ensuing infarcts may be 
simple (mechanical) or septic (with ensuing abscess formation). The 
condition may be suspected when, in the course of the aforementioned 
diseases, sudden pain develops in the region of the spleen, becomes 
aggravated upon motion and respiration, and is accompanied by tender- 
ness, especially on palpation; and when examination discloses enlarge- 
ment of the spleen and perhaps palpable frictions (acute perisplenitis), 



SPLENOMEGALY: SPLENIC ANEMIA 407 

which may be audible on auscultation. Irregular chills, fever, sweats, 
and leukocytosis may be due to the primary infection, or to the develop- 
ment of a splenic abscess. 



ENLARGEMENT OF THE SPLEEN. 

Acute enlargement of the spleen (acute splenic tumor) occurs in many 
infections, notably typhoid fever, malaria, and relapsing fever, in which 
it attains considerable diagnostic significance; but it may be present also 
in septicopyemia, pneumonia, etc.; in acute portal obstruction, in 
embolism and thrombosis of the splenic vein, etc. In venous obstruction 
its cause is obvious; in infection it is attributable to a local congestive and 
inflammatory reaction to the presence of microorganisms or their toxins 
or to toxic paralysis of the vasomotor nerves. Symptoms may be in 
abeyance, although local pain and discomfort may supervene, and on 
examination the spleen may be found enlarged and tender. 

Chronic enlargement of the spleen (chronic splenic tumor) occurs 
in: (1) Passive congestion due to chronic heart disease, chronic liver 
disease (especially cirrhosis), pylephlebitis and other obstructive dis- 
orders of the portal circulation; (2) disorders of nutrition, such as rick- 
ets, amyloidosis, certain obscure (especially tropical) gastro-intestinal 
intoxications, arthritis deformans, etc.; (3) infections, such as malaria, 
syphilis, tuberculosis, kala-azar, and other ill-understood, tropical 
disorders; (4) diseases of the hemopoietic system, such as chlorosis, 
pernicious anemia, leukemia, erythema, Hodgkin's disease, etc.; (5) 
tumors and cysts of the spleen; and (6) certain ill-understood diseases 
discussed under the heading splenomegaly and splenic anemia. The 
enlargement of the spleen per se may not cause any noteworthy symp- 
toms, but local distress and a sense of weight are not uncommon. The 
enlargement is readily disclosed by physical examination. An enlarged 
spleen should not be mistaken for a displaced, though otherwise normal, 
spleen . 

SPLENOMEGALY; SPLENIC ANEMIA. 

In a considerable number of more or less ill-understood disorders 
enlargement of the spleen constitutes a noteworthy feature. The im- 
perfect state of our knowledge precludes a satisfactory classification, 
but several groups of cases may be distinguished: 

1. Congenital or Familial Splenomegaly, with Acholuric Jaundice (Min- 
kowski). This is usually a familial disorder, and may occur in suc- 
ceeding generations. The splenomegaly is often extreme; there is 
slight jaundice, but the stools are not clay-colored, and the urine does 
not contain bile pigments, although it does contain urobilin and uro- 
bilinogen. The blood reveals the changes of secondary anemia. Ne- 
cropsy has revealed chronic hyperplasia of the spleen without cirrhosis 



408 DISEASES OF THE SPLEEN 

of the liver or angiocholitis. The cases must be distinguished from 
those of congenital jaundice in which angiocholitis or obliteration of the 
biliary ducts has been found. The general health often remains notably 
unimpaired. 

2. Congenital or Familial Splenomegaly, with Marked Constitutional 
Disturbances — stunted growth, infantilism, osseous changes, clubbed 
fingers, pigmented skin, enlarged liver, and sometimes jaundice. The 
cases have been encountered especially in children and young adults. 
Whether there is any relationship between these cases and the Min- 
kowski type of acholuric splenomegaly and Hanot's biliary cirrhosis of 
the liver remains to be determined. 

3. Primitive Splenomegaly. This comprises a series of cases charac- 
terized by progressive enlargement of the spleen occurring without known 
cause. In some cases, for many (ten to twenty) years, the general health 
may be scarcely, if at all, impaired, the enlargement of the spleen con- 
stituting the only noteworthy feature of the disease (simple splenomegaly). 
The spleen may reach extraordinary dimensions, extending to the right 
beyond the median line, and far into the pelvis. As a rule, however, 
at the end of three or four years, more or less anemia (splenic anemia) 
supervenes, perhaps attended or preceded by hemorrhages (usually 
hematemesis, but sometimes enterorrhagia, hematuria, epistaxis, menor- 
rhagia, purpura, etc.). The erythrocytes, as a rule, vary from 3,500,000 
to 4,000,000, the color index is low (0.5 to 0.7), and the leukocytes are 
diminished. With the progress of the disease and sometimes in conse- 
quence of recurring hemorrhages, the anemia becomes more marked, 
and, reaching a high grade, may lead to death; exacerbations, as in 
pernicious anemia, are not uncommon. In some cases after the lapse of 
years, signs of portal cirrhosis of the liver (ascites, etc.), associated usually 
with slight jaundice, develop (Banti's disease). The conspicuous lesions 
found in these cases of splenic anemia consist of chronic connective 
tissue hyperplasia of the spleen, leading gradually to atrophy of the 
lymphoid tissue, extraordinary hyperplasia of the endothelial cells of 
the splenic sinuses, and endothelial proliferation and sclerosis (even 
atheroma) of the splenic vein; sometimes similar lesions involve also 
the portal vein, both without and within the liver, and lead to stenosis 
and thrombosis of the branches of the splenic and the portal veins. 
In some cases the proliferation of the endothelium of the splenic sinuses 
constitutes the conspicuous feature of the disease, and has been, though 
incorrectly, interpreted by some observers as related to, if not identical 
with, a tumor formation (splenic anemia or primary splenomegaly of 
the Gaucher type; primitive endothelioma of the spleen) ; identical changes 
may be found also in the liver, lymph nodes, and bone marrow. The 
nature of the disorder is not known, although the splenomegaly is 
assumed to be the primary process; perhaps it develops in consequence 
of some infective or toxic process resident in the spleen, or to the influ- 
ence of which the spleen may be unduly susceptible. This toxin may pro- 
voke the endothelial and other proliferations and ultimately lead to the 



SPLENOMEGALY; SPLENIC ANEMIA 409 

anemia and the hepatic cirrhosis. The undoubted influence of the spleen 
is evident in the prompt recovery and maintenance of health that often 
succeed removal of the spleen before the advent of unalterable changes in 
the liver. 

4. Anemia in Children. In many of the secondary anemias of infants 
and children, such as those due to rickets, syphilis, poor food, faulty 
nutrition, general bad hygienic conditions, etc., as well as the more 
common causes that provoke anemia in adults, the spleen is likely to be, 
although it is not always, enlarged; the enlargement varies much in dif- 
ferent cases. The etiological factor should be sufficiently obvious; 
the blood changes are those of ordinary secondary anemia, although 
a slight leukocytosis is not uncommon; the condition need not be further 
discussed. There are, however, other cases of anemia that develop in 
children without obvious cause and are associated with more or less, 
sometimes considerable, enlargement of the spleen; they are sometimes 
spoken of as the splenic anemias of children. These cases are difficult 
to classify: some observers believe that the primary disturbance is in the 
spleen (the disease being, therefore, akin to the splenic anemia of adults) ; 
others that the splenomegaly is the result of or due to the anemia; others 
that both the anemia and the splenomegaly are the result of a common 
causative factor (perhaps these are allied to pernicious anemia of 
adults) ; and others that some at least of the cases are leukemia or Hodg- 
kin's disease modified in its clinical and anatomical features by the 
young, more or less undifferentiated, or unduly susceptible, hemopoietic 
tissues of infants and children. Several grades of the disorder (or dis- 
orders) may be distinguished: (1) That in which the blood picture 
is that common to secondary anemias (diminished erythrocytes with 
low color index) and a normal number of leukocytes, with perhaps a 
relative lymphocytosis; (2) that differing from the first mentioned 
only in the presence of a moderate leukocytosis (up to 20,000), with little 
if any disturbance in the percentage of the different forms of leukocytes ; 
and (3) that characterized by more marked anemia (3,000,000 or less 
erythrocytes), a variable, sometimes low, sometimes rather high, color 
index, considerable leukocytosis (20,000 to 50,000 or more), poikilo- 
cytosis, anisocytosis, polychromatophilia, megalocytes, megaloblasts, 
and a variable number of myelocytes (20 to 40 per cent, or more), in- 
cluding so-called stimulation forms — the disorder formerly called anemia 
infantum pseudoleukemia of von Jaksch. These three grades doubtless 
often, if not always, represent stages or degrees of the one process, and 
although the causative factor cannot be determined, it is not unlikely 
that some of the cases are due to the sometimes more obtrusive causes of 
ordinary secondary anemia. Recovery may ensue, even when the blood 
contains a large number of myelocytes. The treatment is that of chronic 
secondary anemia. 



410 



DISEASES OF THE SPLEEN 



TUMORS AND CYSTS OF THE SPLEEN. 



Tumors of the spleen may be benign (angioma, fibroma, lymph- 
adenoma) or malignant (sarcoma, endothelioma, carcinoma), and pri- 
mary or secondary. The symptoms consist of local pain and tender- 
ness, enlargement of the organ, which may reveal nodules, and the 
anemia, emaciation, and cachexia common to tumors in general. The 
diagnosis is rarely made before operation (for enlargement), or the 
necropsy. Cysts of the spleen may be simple (serous, hemorrhagic, 
lymphatic), dermoid, or parasitic (echinococcus usually). When large, 
the cyst may cause local distress and reveal itself as a large perhaps 
fluctuating mass. The diagnosis rarely is more than a hazard. 



SECTION VI. 
DISEASES OF THE CIRCULATORY SYSTEM. 



Pathological Physiology. — Studies by Gaskell, Keith, Mackenzie, 
Wenckebach, Hering, His, Erlanger, and others have tended to emphasize 
the importance of the myogenic as contrasted with the neurogenic 
theory of the cardiac action; and although perhaps the two theories 
may yet be found to possess something of truth, the five functions of the 
heart muscle demonstrated by Gaskell and Engelmann constitute the 
basis of the modern conception of cardiac physiology and pathology. 
These are: (1) Stimulus production, the power of producing stimuli that 
excite the heart to contraction; (2) excitability, the power of responding 
to stimuli to contraction; (3) conductivity, the power of transmitting the 
stimulus from one part of the heart to another; (4) contractility, the power 
of contracting in response to stimuli; and (5) tonicity, the power of main- 
taining such contraction of the heart muscle that the total volume of 
the heart and the size of the cavities are less than they would be were 
full relaxation of the muscle to occur during diastole. 

The power of stimulus production seems to be inherent in the muscle 
cells of the heart. The nature of the stimulus is not known, but its 
production is much dependent upon the presence of ionized salts of 
sodium, potassium, and calcium. The stimulus seems to be, as it were, 
a product secreted by the cells and stored until sufficient has been 
produced to excite a contraction. The contraction of the heart depends 
upon its excitability, which disappears immediately the heart has 
contracted; the muscle fibers are said to be in the refractory stage. 
This subsides, that is, excitability returns, during diastole, so that, in 
general, the longer the period of rest the weaker the stimulus that may 
excite contraction. The normal rate and rhythm of the heart are de- 
pendent upon the normal interaction of the two functions of stimulus 
production and excitability. In disease the excitability may be increased 
or diminished. Normally the stimulus to contraction arises in the 
remains of the sinus venosus, the sino-auricular node (of Keith and 
Flack) at the mouth of the superior vena cava (the most excitable 
portion of the remains of the primitive cardiac tube), and it is trans- 
mitted by the muscle fibers (perhaps by the bundle of Thorel) along 
the auricle to the auriculoventricular bundle of His, and thence to the 
ventricles. The regular succession of contractions of the sinus, auricle, 



412 DISEASES OP THE CIRCULATORY SYSTEM 

and ventricle constitutes the normal or sinus rhythm of the heart. In 
disease remains of the primitive cardiac tube other than the sino-auri- 
cular node, becoming unduly excitable, may inaugurate contractions 
(extrasystoles) independently of the sinus rhythm, and the conductivity, 
especially of the auriculoventricular bundle, may become depressed 
(heart block). The power of contractility, the most obvious of the 
heart actions, is peculiar in that each contraction is maximal and is 
followed by a long refractory period. The fact of the contraction being 
maximal, that is, as powerful as the heart is at the time capable of, 
renders the heart independent of the strength of the stimulus, insures a 
forceful response (contraction) to a weak stimulus, and prevents an 
excessive response to a strong stimulus; the refractory period insures 
a period of rest and renders tetanization of the muscle impossible. In 
general the strength of the contraction is proportional to the duration 
of the immediately preceding period of rest. The power of contractility 
may become much depressed in disease. Tonicity is a property possessed 
by the cardiac musculature in common with muscular tissue elsewhere 
in the body; it keeps the volume of the heart and the size of the cavities 
somewhat less than they would be were full relaxation of the muscle to 
occur during diastole. It is the force, therefore, that opposes dilatation; 
it varies much in different individuals in health and disease; it may be 
increased by drugs, such as digitalis; and it may be diminished by drugs, 
such as muscarin, and by the toxins of infectious diseases. Depression 
of tonicity is the obtrusive manifestation of failure of the heart. The 
coordinated activity of all the functions of the heart is essential to the 
maintenance of the efficiency of the circulation, and this coordinated 
activity in turn depends upon a sufficiency of nutriment. 

In studying diseases of the heart and interpreting their manifestations, 
it is essential to have in mind not only the myocardium and its nervous 
control exerted by way of the pneumogastric and the accelerator nerves, 
but also its vascular or vasomotor control exerted through the elasticity 
and contractility of the bloodvessels. This is of importance because 
of its bearing upon the blood pressure, which is the resultant of the 
resistance in the arterioles (controlled by the vasomotor nerves), of 
the elasticity of the arterial walls, of the force of the heart beat, and of the 
volume of blood. Without discussing the subject at length, it perhaps 
suffices to point out that the circulation may fail at the periphery as well 
as at the heart, and that this is more often the case than is. usually sup- 
posed — as in shock generally, in the heart failure (more properly vaso- 
motor failure) of many infectious processes, etc. Furthermore the 
beginnings of serious cardiovascular disease are often in the periphery; 
here divers endogenous and exogenous poisons exert their deleterious 
influence, and in consequence of a direct irritant action on the vaso- 
motor nerves, or perhaps on the muscular coat of the vessels, increase 
the blood pressure, and inaugurate the series of changes discussed 
under arteriosclerosis. It is essential, therefore, to study the arterial, 
the capillary, the venous, and the pulmonary circulation. 



PATHOLOGICAL PHYSIOLOGY 413 

In all diseases of the heart the major factor to be determined is the 
functional capacity of the heart, in comparison with which other matters 
are of minor significance. Noteworthy incapacity of the heart is quite 
obvious in symptoms of unstable compensation or of impending or 
actual decompensation; of these, several, such as cardiac pain, palpita- 
tion, irregularities of rate and rhythm, etc., are discussed under the general 
heading of neuromuscular disorders. There are several others, common 
to the different forms of heart disease, such as dyspnoea, cyanosis, and 
oedema, that plainly disclose the functional incapacity, the functional 
failure, of the heart. 

Dyspnoea is very common; it may be the only symptom, but is 
often accompanied by a sense of precordial or substernal distress or 
actual pain, and more or less anxiety and apprehension; and it 
varies much in degree from slight breathlessness on exertion or excite- 
ment to orthopncea even when the patient rests in bed. This dysp- 
noea is due directly to deficient oxygenation of the blood — to an excess 
of carbon dioxide, which in turn results from a slow and feeble circula- 
tion; the excess of carbon dioxide acts as an irritant to the respiratory 
centre in the medulla and increases the respiratory rate. Contributing 
factors are often present, such as chronic passive congestion with result- 
ant changes in the alveolar epithelium and encroachment upon the 
interalveolar space in consequence of dilatation of the capillaries, loss 
of elasticity of the lungs, oedema of the lungs, chronic bronchitis, 
bronchopneumonia, etc. The dyspnoea sometimes comes on paroxys- 
mally in attacks — so-called cardiac asthma. These attacks are due to 
temporary incapacity of the left ventricle, which may be provoked by 
exertion, excitement, a full meal, flatulence, constipation, etc., or the 
attacks may come on without obvious cause. They are quite common 
early in the night, developing soon after the patient has fallen asleep. 
Sometimes, especially in arteriosclerotic subjects (cardiovascular-renaj 
disease) with involvement of the brain, the respirations are peculiarly 
periodical, longer or shorter periods of apncea alternating with 
periods of breathing, at first slow and shallow, but gradually becoming 
deeper and more rapid until they reach a maximum, whereupon 
they gradually decrease and finally again cease (Cheyne-Stokes breath- 

in g)- 

Cyanosis attends dyspnoea and is due to like causes — to an excess o\ 

carbon dioxide in the blood. In chronic cases the patients not infre- 
quently become more or less accustomed to the cyanosis, the organism 
adapts itself to the changed conditions, and although the cyanosis may be 
more or less obvious, there may belittle or no subjective dyspnoea, and 
the functions of the body may be fairly well performed. Cyanosis 
occurs not only in diseases of the heart, but also in diseases of the lungs 
interfering with proper oxygenation of the blood; in erythremia (poly- 
cythemia with cyanosis and enlarged spleen); rarely in conditions due 
to alteration of the blood pigment itself: that is, the conversion of the 
hemoglobin into metahemoglobin (chronic poisoning by acetanilide, 



414 DISEASES OF THE CIRCULATORY SYSTEM 

phenacetin, sulphonal, trional, etc.); and in so-called enterogenous 
cyanosis (intestinal auto-intoxication), due in one series of cases to con- 
version of the hemoglobin into methemoglobin, the result of the absorp- 
tion of nitrites from the intestine in chronic diarrhoea, and amenable 
to a milk diet, and due in another series of cases to conversion of the 
hemoglobin into sulph-hemoglobin, the result apparently of putre- 
faction of the proteins in chronic constipation (increased formation 
or absorption of H 2 S), and amenable to treatment directed toward the 
constipation. 

The oedema of cardiac disease is largely the result of slowing of the 
circulation and consequent stasis of the blood; but changes in the 
endothelium of the capillary blood vessels and lymph spaces are a con- 
tributing factor. This oedema from stasis is to be distinguished from so- 
called inflammatory oedema, nephritic oedema, and hydremic oedema. 

In many cases of readily recognized heart disease, compensation has 
not failed, nor is it unstable; but it is nevertheless desirable to ascertain 
the functional capacity of the heart. This may be roughly determined 
by noting the amount of work or excercise that provokes dyspnoea, 
palpitation of the heart, precordial distress, and increased frequency 
of the heart beat; but this is a rude test. Other more or less accurate 
and satisfactory methods of determining the functional capacity of the 
heart have been suggested. The graphic methods, especially emphasized 
by Mackenzie, whereby it is possible to recognize disturbances of excita- 
bility, conductivity, contractility, tonicity, and rhythmicity, are excellent; 
but are not often available in clinical work outside a hospital. Other 
methods are based upon the changes in blood pressure and pulse rate 
provoked by a measured amount of work. A simple test consists in 
determining the difference between the rate of the heart beat in the 
erect and in the recumbent posture; normally recumbency produces a 
lessening of the heart beats of from six to twenty per minute; this is 
partly or completely lost in cardiac insufficiency. Mendelsohn has 
suggested that the functional capacity of the heart may be estimated 
by ascertaining the time required for the heart to regain its normal 
rate after a measured amount of work. Katzenstein determines the 
blood pressure and the pulse rate after digital compression of both 
femoral arteries. In normal individuals this compression results in 
an increase of the systolic blood pressure in the brachial artery of 
from 5 to 15 mm. Hg., without noteworthy changes in the pulse rate; 
in cases of efficient hypertrophy the blood pressure may be increased 
15 to 40 mm. Hg. ; in cases of slight cardiac insufficiency, the pressure 
may not rise at all, while the pulse rate becomes accelerated; and in 
cases of marked cardiac insufficiency the blood pressure may fall and the 
pulse rate become accelerated. The pain and mental excitement induced 
by the procedure seriously compromise the results, and a marked in- 
crease in blood pressure is not entirely free from danger. Graupner has 
drawn attention to the fact that after a measured amount of work 
the systolic blood pressure and the pulse rate thus increased, gradually 



NEUROMUSCULAR DISORDERS OF THE HEART 415 

return to the normal, and that after the pulse rate has declined to the 
normal the systolic blood pressure begins to rise, attains its maximum 
several minutes later than the pulse rate, and then falls to (or below) 
the normal; this so-called normal recovery may be delayed and di- 
minished in slight cardiac inadequacy, and it may be entirely absent in 
marked cardiac insufficiency, the blood pressure declining continuously, 
and only reaching the normal after a longer or shorter period of rest. 
Stair climbing or lifting weights, may be resorted to for the measured 
amount of work. 



NEUROMUSCULAR DISORDERS OF THE HEART. 

Disturbances in the sensory or motor activities of the heart often either 
dominate the clinical picture or constitute the sole discoverable evidence 
of cardiac disease. These disturbances, in consequence, are often spoken 
of as neuroses or functional disorders of the heart, terms that have some 
justification in fact, but are often misnomers, since the disorders in 
question often constitute mere symptoms or symptom-complexes and 
have an anatomical basis. Convenience, however, and the grouping of the 
phenomena suggest their discussion together under the designation neuro- 
muscular or symptomatic disorders. These may be divided into the 
sensory and the motor. The sensory disorders are represented by cardiac 
pain and distress and the subjective sensations associated with palpita- 
tion and with some forms of irregularity or intermission of the heart; 
the motor disorders include disturbances of rate (rapid, infrequent; 
tachycardia, bradycardia), of rhythm (the different types of arrhythmia), 
and of force (strong and weak). 

Cardiac Pain. — Cardiac pain varies much in character, intensity, 
and in situation. It may be a mere discomfort, or an actual pain — dull, 
aching, stabbing, or agonizing, griping, constricting, vise-like. It may 
be referred to the apex of the heart, to the entire precordium, to the 
axillae, and it may radiate to the back, to one or both arms, etc. The 
agonizing, constricting, vise-like pain of angina pectoris is, of course, the 
obtrusive manifestation of the disorder; but since the disorder has an 
anatomical basis, it should not be called a neurosis. 

Cardiac pain may be due to organic or so-called functional disorders 
of the heart: (1) The organic cases comprise all the diseases of the 
myocardium, endocardium, and pericardium, and of the aorta, thai 
will be discussed under the respective headings. (2) Other cases are 
due to the toxic action of tobacco, alcohol, tea, coffee, etc., and may or 
may not be associated with demonstrable organic changes; the pain or 
distress usually ceases in the course of time upon discontinuance of the 
exciting factor. (3) A third group of cases are the so-called nervous 
cases; cases induced by shock, emotional disturbances, excessive venery, 
etc.; or associated with neurasthenia, hysteria, disorder of the genitalia 
(male and female) or of the kidneys, etc.; or apparently due to disorder 



416 DISEASES OF THE CIRCULATORY SYSTEM 

of the vasomotor system (NothnagePs vasomotor angina). (4) Some 
cases are due solely to gastro-intestinal derangements associated with 
flatulence; they are readily cured by attention to the exciting cause. 

Palpitation of the Heart. — In health the activity of one's heart is 
entirely unnoticed; the subjective consciousness of the heart's pulsation, 
so-called palpitation, develops under a variety of circumstances. It is a 
normal phenomena under the stress of unusual exertion or excitement, but 
the sensations of throbbing thus experienced are perfectly regular, as a 
rule, and soon subside with the initiating cause. It develops upon slight, 
sometimes very slight, provocation in cases of unusual excitability of the 
nervous system, in neurasthenia and hysteria; and in women generally 
rather than in men, especially at times of nervous perturbation, as at 
puberty, during menstruation, at the climacteric, and in conditions of 
worry, anxiety, and emotional disturbances. It occurs also in con- 
sequence of the toxic influence of tobacco, alcohol, tea, coffee, etc., 
on the heart; in the myocardial degenerations associated with anemic 
conditions and the acute infections; in the condition of irritable heart, 
due to excessive muscular strain; in organic (myocardial and endocardial) 
diseases of the heart generally; and in many disorders of the abdominal 
organs, notably flatulent dyspepsia. 

The attacks vary much in severity — from a slight and transitory feeling 
of fluttering of the heart to severe spells of very forcible throbbing of the 
heart, attended by marked precordial distress or oppression, that may 
continue for an hour or more. The throbbing not infrequently extends 
to the arteries and may lead to flushing of the skin and perhaps to 
perspiration and transient polyuria. Usually the heart's action is much 
accelerated, up to 150 or more per minute, and often irregular; but 
occasionally the rate and rhythm are quite normal; and on the con- 
trary some attacks of very rapid heart action (delirium cordis) may 
be entirely unperceived by the patient. Examination of the heart, as a 
rule, reveals only the evidence of the hyperactivity. The sounds usually 
are normal or perhaps somewhat accentuated, especially the pulmonary 
second sound. There may be a slight systolic murmur in the pulmonary 
area, especially in the anemic and neurasthenic cases. 

Arrhythmia. — The following varieties of arrhythmia may be dis- 
tinguished : 

1. Respiratory Arrhythmia (Juvenile Arrhythmia; Sinus Irregularity 
Mackenzie). — Respiratory arrhythmia is an exaggeration of the normal 
inspiratory increase and expiratory decrease in the frequency of the cardiac 
action ; it is characterized by variations in the duration of the cardiac cycle, 
dependent almost if not quite wholly upon prolongation of the diastole. 
It is not associated with noteworthy changes in the size of the individual 
pulse beats, nor is it a condition of missed beats at the wrist due to extra- 
systoles. It is not uncommon in youths approaching puberty, but rarely 
occurs in healthy adults; it is sometimes observed during convalescence 
from acute infections (diphtheria, scarlet fever, typhoid fever, pneumonia, 
etc.), in anemic conditions, in neurasthenia, in cerebral disorders, tuber- 



NEUROMUSCULAR DISORDERS OF THE HEART 417 

culous meningitis, etc. It is often associated with slowing of the heart 
action and infrequent respiration, and is attributable to irritation of the 
vagus (exaggeration of the normal respiratory reflex). It is readily recog- 
nized: beats of equal strength varying continually in time with the phases 
of respiration, being, as a rule, most infrequent during expiration. 
Occasionally in children it may be mistaken for continuous irregularity 
(nodal rhythm), but it may be distinguished by a tracing of the jugular 
vein which shows concurrent involvement of the auricle, and by its 
being lessened or dissipated by atropine (which does not influence con- 
tinuous irregularity), and by being increased by digitalis (which lessens 
continuous irregularity). It should not be confused with the parodoxic 
pulse — inspiratory diminution in the force and volume of the pulse. 
Of itself it is of minor significance and good prognosis, and it calls for 
no special treatment. 

2. Extrasystoles. — The majority of cases of arrhythmia are due 
to extrasystoles, that is, to "premature contractions of the auricle or 
the ventricle in response to a stimulus from some abnormal point of the 
heart, but in which otherwise the fundamental or sinus rhythm of 
the heart is maintained" (Mackenzie). Mackenzie reasons that, since the 
stimulus for contraction arises normally in the remains of the sinus 
venosus at the mouths of the great veins (the sino-auricular node), 
other remains of the primitive cardiac tube, if rendered more excitable, 
might start the contraction before the sinus; and since this primitive 
cardiac tube in the heart is represented also in the auricle, in the auriculo- 
ventricular node, and in the auriculoventricular bundle after it leaves 
the node, he (as well as others) describe the following types of extra- 
systoles : 

1. Ventricular extrasystoles, those in which the origin of the 
extrasystole is assumed to be in the auriculoventricular bundle beyond 
the f auriculoventricular node (that is, in the ventricle). This stimulates 
the ventricle to contraction in advance of the normal time; this contrac- 
tion (extrasystole) is followed by the usual refractory period which 
extends beyond the time that the normal stimulus from the sino-auric- 
ular node reaches the ventricle; the ventricle in consequence remains 
inactive, a beat is missed, and a large so-called compensatory pause 
ensues, which is terminated by a forcible (maximal) contraction of the 
ventricle in response to the next ensuing stimulus from the auricle; this 
occurs at the proper time and in normal rhythm. Characteristic of the 
ventricular extrasystole is the fact that the time occupied by the normal 
systole, the extrasystole, and the compensatory pause is twice that of a 
normal cardiac cycle; the number of heart beats per minute may remain 
normal, a premature ventricular systole (extra-systole) being inter- 
polated between two normal contractions. 

2. Auricular extrasystoles, those in which the stimulus is assumed 
to arise in the remains of the primitive cardiac tube incorporated in the 
auricle elsewhere than at the sinus. As in the ventricular extrasystoles, the 
premature contraction of the auricle (extrasystole) is followed by a con- 

27 



418 DISEASES OF THE CIRCULATORY SYSTEM 

traction of the ventricle; but the normal stimulus from the sinus finds 
the auricle refractory and contraction does not take place. This form of 
arrhythmia resembles ventricular extrasystoles, and usually is distinguish- 
able only by tracings of the jugular pulse (which reveal the auricular 
extrasystole) . As in ventricular extrasystoles the time occupied by the 
normal systole, the extrasystole, and the long pause may be twice that of 
a normal cardiac cycle; but in most cases it is less; that is, the pause 
is not compensatory. 

3. Auriculoventricular extrasystoles (nodal extrasystoles), those 
in which the stimulus is supposed to arise in the auriculoventricular 
node of Tawara, and gives rise to premature and simultaneous con- 
tractions of auricles and ventricles. This is assumed by some ob- 
servers to be a so-called retrograde extrasystole, that is, a ventricular 
extrasystole in which the stimulus has travelled back along the auriculo- 
ventricular bundle and prematurely stimulated the auricle, an assump- 
tion that Mackenzie believes untenable. 

Extrasystoles result from the increased excitability of the remains of 
the primitive cardiac tube (Mackenzie); perhaps occasionally from an 
exaggeration of the normal automatism of the heart. Mackenzie believes 
that the compensatory pause is not due to the ventricle being refractory, 
but to the auriculoventricular bundle being refractory (impaired conduc- 
tivity), and not conveying the stimulus to the ventricle, which, therefore, 
stands still until the next physiological stimulus comes down from the 
auricle. Clinically this type of arrhythmia is characterized by the occur- 
rence of two or more approximated pulse beats followed by an unusually 
long pause (intermission of the pulse). The extrasystole may occur only 
at long, irregular intervals, at short irregular intervals, or at short regular 
intervals, as after every second beat, every three beats, etc., in which latter 
event it gives rise to the so-called bigeminal, trigeminal, quadrigeminal, 
quinquegeminal pulse, etc. A continuous series of extrasystoles may 
give rise to a type of paroxysmal tachycardia (usually, however, this is 
of the nodal rhythm). In some cases the extrasystole is more or less 
ineffectual, because it occurs early in diastole (in the refractory period, 
when the ventricle is incapable of much contractile effort), the ventricle 
contains very little blood, and the pressure in the aorta is very high — so 
that the aortic leaflets are opened slightly, if at all. This more or less 
ineffectual extrasystole produces little if any perceptible influence on the 
pulse (although it may be registrable on the sphygmogram or cardio- 
gram); the pulse then appears to be definitely intermittent — a beat is 
missed. If this occurs with regularity after each normal systole of the 
ventricle, the condition at first may be mistaken for bradycardia, which, 
however, can be differentiated by tracings of the jugular pulse or of the 
apex beat, and by auscultation. There is some doubt as to the occurrence 
of hemisystole (alternate contraction of the two ventricles). Mackenzie 
and Hering believe that most reported cases are really cases of extra- 
systole, and that hemisystole occurs only in a dying heart; von Leyden, 
Kraus, and Nicolai believe, however, that rarely the ventricles may act 



NEUROMUSCULAR DISORDERS OE THE HEART 419 

asynchronously. On auscultation the extrasystole, if it occurs early in 
diastole and is ineffectual in opening the aortic valve, is revealed bv a 
single, usually a muffled, sometimes a loud, sound; if it occurs later in 
diastole, and does lead to opening of the aortic valve, a second sound 
may also be produced; the two normal sounds are quickly followed by 
two weaker sounds and an unusually long pause. Subjects are some- 
times conscious of the extrasystole — a dull thud in the region of the 
precordium, or a sensation of stoppage of the heart and a palpable 
intermission of the pulse. Although, as a rule, readily recognizable, 
it is sometimes difficult to distinguish extrasystoles ; the several types 
may occur in varying combinations, and they may be associated with 
other forms of arrhythmia. 

Extrasystoles occur in a variety of conditions: (1) In neurotic subjects, 
especially after exertion and excitement, at puberty, and the climacteric, 
during pregnancy, in hysteria, neurasthenia, etc., and reflexly in indi- 
gestion and divers gastro-intestinal disorders; (2) in toxic conditions 
such as those due to tobacco, tea, coffee, alcohol, etc. ; (3) in infections, 
especially during convalescence from typhoid fever, pneumonia, diph- 
theria, scarlet fever, etc.; and (4) in the various sorts of acute and 
chronic diseases of the heart, especially those associated with hyper- 
tension. In themselves, extrasystoles are of minor clinical significance, 
of which fact the patient, if aware of the irregularity, should be assured ; 
the associated conditions, such as infections and various sorts of heart 
disease, may be of great significance, even dangerous. The treatment 
should be directed to the associated or underlying factors. 

3. Continuous Irregularity (Perpetual Irregularity; Nodal Rhythm; 
Rhythm of Auricular Paralysis; Ventricular Rhythm; Absolutely Irregular 
Heart). — This is characterized by irregularity in the force, equality, and 
sequence of the pulse beats, by the absence of the fundamental or sinus 
rhythm of the heart, by the presence of a ventricular (or positive) venous 
pulse (tricuspid insufficiency or auricular paralysis), by the absence of 
an auricular wave on the jugular tracing, and by the permanence of 
the phenomena. The cardiac action may be extremely rapid (delirium 
cordis); occasionally it may be very rapid temporarily (paroxysmal 
tachycardia); rarely it may be quite slow, especially under the influence 
of digitalis; except when very rapid, the cardiac action is always irregular 
and this maybe of minor or of high grade. The auscultatory phenomena 
are similarly irregular: the sounds vary in character and intensity, many 
of the systoles are not followed by second sounds, and they occasion no 
palpable pulse at the wrist. 

The condition is due to the concurrent contraction of the auricle 
and the ventricle (sometimes antecedent contraction of the ventricle), in 
response to stimuli arising at the auriculoventricular node (Mackenzie), 
or to a block between the sinus and the auricle (depression of conduc- 
tivity, Wenckeback, Erlanger). It is found in all forms of severe hear! 
failure with dilatation of the auricles, particularly those of rheumatic 
origin (mitral stenosis especially) and the fibroid heart. Mackenzie 



420 DISEASES OF THE CIRCULATORY SYSTEM 

believes that in a great many cases the immediate breakdown is directly 
attributable to the inception by the heart of the abnormal rhythm. 
The condition is always of serious moment. When once established 
it usually continues until death, although it may be improved by appro- 
priate treatment, especially the use of digitalis; that is, some normal 
beats occur and irregular beats become less apparent; but evidence of 
auricular contractions usually do not again become evident, and slight 
exertion sets up extreme irregularity and rapid action of the heart. 

4. Partial and Complete Heart Block (Depression of Conductivity). — 
In some cases, the ventricle fails to contract after each auricular 
contraction, in consequence of failure of the auriculoventricular 
bundle of His to conduct the stimulus to the ventricle ; the condition, 
therefore, is a manifestation of depressed conductivity, and is spoken 
of as partial or complete heart block. But depression of conductivity 
may occur without arrhythmia. Erlanger has shown experimentally 
that varying degrees of compression result first in increase of the inter- 
systolic period (a-c interval; that is, the time between the beginning of the 
auricular and the carotid waves in tracings of the jugular pulse); then in 
a 2 to 1, 3 to 1, or 4 to 1 auriculoventricular rhythm (incomplete heart 
block); and finally in independent auricular and ventricular contrac- 
tions (complete heart block). Mackenzie states that the stimulus to the 
ventricle may be, (1) delayed; (2) prevented from crossing the bundle 
of His; or (3) completely blocked beyond the auriculoventricular node, 
in which event the ventricle contracts in response to a stimulus that 
arises in the uninjured remains of the auriculoventricular bundle 
(heart block, ventricular rhythm). Clinically the condition is mani- 
fested by a slow ventricular rate (slow radial pulse ; one type of brady- 
cardia), associated with more frequent pulsations of the veins of the 
neck, owing to preservation of the normal rate of auricular contractions. 
If the ventricular contractions are more than thirty-six per minute, 
they may have a distinct relationship to the auricular waves in the 
jugular pulse, the ventricle responding to every second, third, or fourth 
auricular contraction; when the ventricular contractions are about 
thirty or less, they are probably independent of the auricle, and the auricle 
and the ventricle beat at independent rates, in response to independent 
stimuli. The condition may be suspected when there is a complete pause 
in the radial pulse with absence of heart sounds (Mackenzie). 

Temporary and incomplete heart block occurs rarely in certain infec- 
tions (or during convalescence), such as typhoid fever, pneumonia, 
diphtheria, scarlatina, rheumatism, influenza, etc.; it may occur in the 
fibroid heart; and it may be set up by the prolonged use of digitalis. 

Complete heart block is typically represented in the so-called Adams- 
Stokes syndrome, of which the characteristic features are: (1) Brady- 
cardia, sometimes permanent, sometimes paroxysmal and temporary, 
the radial pulse and the ventricular systoles falling to 40, 20, 10 or less, 
a minute ; (2) visible auricular pulsation of the veins of the neck due to 
auricular contractions, and often revealing a 2 to 1, 3 to 1, or 4 to 1 



NEUROMUSCULAR DISORDERS OF THE HEART 421 

rhythm as compared with the ventricular contractions; and (3) cerebral 
(anemic) disorders — vertigo, syncope, pseudo-apoplectiform attacks, 
sometimes associated with convulsions (epileptiform) of variable severity 
and duration. The cases of heart block that have been carefully 
studied after death have revealed more or less destructive lesions, espe- 
cially gummas, sclerosis, atheroma, anemic necrosis, etc., of the auriculo- 
ventricular bundle of His, sufficient partly or completely to interrupt 
the conduction of impulses. It is surmised that the less degrees of heart 
block are due to less-marked, in some cases perhaps merely functional 
lesions of the bundle. The cases due to digitalis are the result of a 
specific depressive action of the drug on the function of conductivity. 
The Adams-Stokes syndrome is a serious malady, ultimately fatal, 
although it may last for years. The use of the iodides often leads to 
marked improvement, especially in the syphilitic (gummatous) cases. 
Strychnine also has proved of avail. 

5. Alternating Pulse (Depression of Contractility). — The alternating- 
pulse consists of a regular succession of large and small pulse 
waves, and results from depression of the function of contractility. 
Mackenzie states that "when contractility is depressed, if time be allowed 
for a full and strong contraction, the longer duration of contraction 
encroaches upon the period of rest, so that by the time the next stimulus 
arrives the contractility has not sufficiently recovered, and a smaller and 
shorter contraction results. As this contraction is shorter in duration, 
the period of rest is thereby lengthened before the next stimulus arrives, 
so that the contraction will be stronger and longer; being longer, it will 
again encroach upon the period of rest, and so the process of alternation 
goes on." This alternating pulse is found in conditions of exhaustion 
of the myocardium, especially in advanced mitral stenosis, coronary scle- 
rosis, general arteriosclerosis with high blood pressure, angina pectoris, 
fibroid heart, etc. It is of serious moment. 

Tachycardia.— The term tachycardia is more or less loosely applied to 
abnormal frequency of the heart action; by some observers the term is 
restricted to extraordinary frequency (twice the normal — 150 or more); 
and it is not infrequently confused with the term paroxysmal tachy- 
cardia, which seems to be a distinct clinical entity. Abnormal frequency 
of the pulse may be physiological or pathological. The physiological 
cases comprise those normal individuals in whom the pulse is persistently 
above the average of normal persons — 80 to 100 per minute. The 
pathological cases comprise those due to: (1) Infections, which include 
almost all the infectious diseases, in which, associated with fever, the pulse 
becomes accelerated. In perhaps the majority of cases the acceleration 
of the pulse is proportionate to the increment of fever; in some cases, 
notably scarlatina, the pulse is disproportionately rapid; while in others 
such as typhoid fever, certain forms of meningitis, although it may be 
of increased frequency, this is not up to the average of other fever states ; 
in some of these cases the pulse may even be slowed. (2) Intoxications, 
such as tobacco, tea, coffee, atropine, strychnine, alcohol, etc. (3) All 



422 DISEASES OF THE CIRCULATORY SYSTEM 

acute and chronic diseases of the heart, such as irritation, overstrain, 
valvular diseases (notably mitral stenosis), myocardial disease, peri- 
cardial disease, etc., especially in impending or actual decompensation. 
(4) Neurotic disturbances, such as emotional and other shocks, hysteria, 
neurasthenia, and some organic nervous diseases. (5) Graves' disease. 
(6) Paroxysmal tachycardia. 

Paroxysmal tachycardia is a disorder characterized by paroxysms 
of extraordinary frequency of the heart beat and the pulse. It occurs 
in both sexes, especially in neurotic individuals, and in subjects with pre- 
viously normal hearts, as well as in cardiopaths. It commonly develops 
in adult life, although it may come on during childhood. It is usually 
attributed to paralysis of the inhibiting centre (vagus), but minor grades 
(a pulse rate of less than 120) are sometimes ascribed to irritation of the 
sympathetic. Mackenzie regards the condition as a manifestation of 
extrasystoles (transient and recurrent nodal rhythm). The attacks 
come on suddenly, usually without obvious cause, last several minutes, 
several hours, or several days, and usually end abruptly; they may recur 
at irregular intervals, days, weeks, months, or years; or perhaps there 
may be only the one attack. The attack is characterized by subjective 
sensations of oppression, tightness, or fluttering in the region of the 
heart, associated with restlessness and weakness, and often dyspnoea on 
exertion. The pulse is found to be small and rapid, often 200 or more 
per minute (sometimes so rapid that it cannot be counted); often there is 
no noteworthy inequality in the force, rhythm, or volume of the beats, 
but more or less (even marked) arrhythmia may develop. Auscultation 
reveals the heart sounds to be short and sharp (embryocardia; tic-tac), 
and often a systolic murmur (mitral insufficiency). The heart may 
become markedly dilated, even within a short time (according to Martius, 
the disorder is a recurring acute dilatation of the heart), and the veins of 
the neck and the liver may become distended and pulsate. The prog- 
nosis depends upon the functional capacity of the heart under the 
abnormal rhythm, upon the general circulatory conditions under the 
new circumstances. Dyspnoea and oedema are of bad prognostic 
significance. Mackenzie believes that many cases of rapid and fatal 
breakdown, particularly in old people, are due directly to the inception 
by the heart of this rhythm. The treatment comprises bodily rest and 
mental quietude, under which some attacks subside spontaneously. The 
bromides, morphine, valerian, and other sedatives may prove of service; 
belladonna, the iodides, nitroglycerin, etc., have been recommended 
from time to time. Attacks sometimes may be stopped by the patient 
taking a long breath or a series of long breaths and fixing the chest in 
full inspiration, by the use of ice-cold douches to the chest, by irritation 
of the vagus nerve in the neck (pinching, faradization, etc.). 

Bradycardia.— The term bradycardia is more or less loosely applied 
to abnormal infrequency of the pulse; supposedly the cardiac action is 
at the same time infrequent, but in reality this is not always so. Follow- 
ing Mackenzie, the cases of diminished frequency of the pulse may be 



DISEASES OF THE MYOCARDIUM 423 

divided into four classes: (1) Those in which all the chambers of the 
heart participate in the slow action (true bradycardia); (2) those in 
which the slow pulse rate is due to a missed beat, the ventricle having 
contracted but the resulting pulse-wave being too feeble to reach the 
wrist (extrasystolic form of arrhythmia); (3) certain cases of nodal 
rhythm in which the auricle has ceased to beat, or beats synchronously 
with the ventricle (mild heart block) ; and (4) cases in which the stimulus 
is blocked between the auricle and the ventricle so that the auricle beats 
at its normal rhythm and the ventricle does not respond to the auricular 
systole, but pursues an independent and slow rhythm (complete heart 
block). The cases are due then to stimulation of the vagus (inhibition), 
or to depressed conductivity and contractility of the myocardium. 

True bradycardia may be physiological or pathological. The physio- 
logical cases comprise certain normal individuals in whom the pulse is 
always abnormally slow — 60 or less; the pulse may become slowed also 
during pregnancy, less than 60, even 50, 40, or less, and in starvation 
(but this perhaps verges on the pathological). The pathological cases 
comprise those due to: (1) Infections, such as typhoid fever, pneumonia, 
diphtheria, influenza, rheumatism, etc., in convalescence from which 
it is rather common; (2) intoxications, such as alcohol, coffee, tea, lead, 
tobacco, uremia, digitalis poisoning, etc.; (3) disease of the heart, 
especially the fatty heart, chronic myocarditis, aortic stenosis, etc. ; (4) dis- 
orders of the lung, especially emphysema; (5) divers disorders of the 
gastro-intestinal tract, such as gastric carcinoma, jaundice, cholelithiasis 
(especially during colic), etc.; (6) nervous disorders, such as apoplexy, 
meningitis, brain tumor, injury of the medulla, vagus stimulation by 
tumors, coma, epilepsy, etc.; and (7) anemic, cachetic, and exhausting 
disorders of wide diversity. In true bradycardia the pulse rate is rarely 
less than 40. The condition is not serious; it may last for many years. 
The use of atropine, since it accelerates the cardiac activity in the vagus 
cases, may help to distinguish these from the myocardial cases. 



DISEASES OF THE MYOCARDIUM. 

In the introductory remarks on the pathological physiology of the 
cardiovascular system the prime importance of the myocardium has been 
emphasized, and later certain disorders to which the myocardium is 
subject under divers circumstances have been grouped together under 
the designation neuromuscular disorders. An attempt to separate 
diseases of the myocardium and to discuss them apart from other diseases 
of the heart, however, is a matter of extreme difficulty, if not impossibility. 
The relationships that the myocardium, in health and in disease, bear 
to the normal and the perverted activity of the heart are so intimate 
that one can scarcely be thought of independently of the other. What- 
ever the disorder of the heart under consideration, the major diagnostic, 
prognostic, and therapeutic considerations must be based upon the 



424 DISEASES OF THE MYOCARDIUM 

condition of the myocardium. In chronic valvular disease, for instance, 
although the condition of the valves or orifices is of significance, the 
efficiency of the circulation, the comfort of the patient, and the dura- 
tion of life depend upon the functional capacity of the myocardium under 
the new or changed conditions; this is true also in diseases of the peri- 
cardium, notably in chronic adhesive pericarditis, and likewise one may 
also say in the advanced anemic and cachetic stages of general disorders 
in which degenerative changes in the myocardium are prone to develop. 
The classification of diseases of the myocardium, therefore, is exceed- 
ingly intricate; no classification is entirely satisfactory. It is even 
difficult to draw a line between the primary and the secondary diseases 
of the myocardium. Hypertrophy and dilatation, for instance, are due 
to many factors, each more or less separate and distinct in itself and 
productive of varying grades of mischief; bacterial toxins, chemical 
poisons of widely diverse nature, and anemic conditions may engender 
degenerative changes in the myocardium that may be expressed in 
myocardial weakness or dilatation, the phenomena of which may domi- 
nate the clinical picture; the fibroid heart may be viewed as a disease of 
the myocardium or of the coronary arteries, to which in the great majority 
of cases it is directly due; and, finally, the nutrition of the heart under 
all conditions, its functional capacity, its ability to hypertrophy under the 
stress of unusual demands, its failure to adapt itself to new or changed 
conditions, etc., are due wholly to the condition of the coronary circula- 
tion — generally as well as locally. In the absence of a satisfactory 
classification, the subjoined arrangement of diseases of the myocardium, 
may be adopted tentatively; it comprises more or less well-defined 
clinical entities with associated pathological changes, which, however, 
gradually merge into other conditions. 



THE WEAK OR INSUFFICIENT HEART. 

(Myocardial Weakness or Insufficiency; Congenital Weakness of the Myocardium; 
Acquired Weakness of the Myocardium; Cardiac Asthenia.) 

Etiology. — There is a more or less diversified group of disorders of 
the heart, of which the pathological lesions are inconspicuous, and of 
which the noteworthy clinical manifestation is myocardial weakness; 
the other clinical manifestations and the etiological factors may be 
quite dissimilar. These disorders, therefore, not only differ more or 
less among themselves, but they cannot be sharply separated from other 
disorders of the myocardium. Unquestionably some of these cases are 
congenital: the subject is born with a "weak heart;" other cases are 
acquired. In the congenital cases the weakness occasionally is more 
or less obviously represented in smallness in the size of the heart or in 
thinness of its walls; often the structure is apparently normal, but the 
organ is physiologically inadequate; in either event the heart is unable 
to meet the requirements of ordinary life. The acquired cases result 



THE WEAK OR INSUFFICIENT HEART 425 

from damage to a heart originally normal. The important etiological 
factors are: (1) The infectious diseases. In these disorder of the heart 
may develop as described under the infectious febrile heart; usually 
the heart returns to its previously normal condition, but it may remain 
for some time or permanently weak or insufficient. (2) Intoxicants — 
such as alcohol, tobacco, coffee, tea, etc., especially when taken in 
excess. (3) Anemic and cachectic states. (4) Neurotic disturbances, 
exemplified in undue reaction to emotional and extraneous influences, 
or in general nervous incapacity with special involvement of the heart. 
In some cases the damage is doubtless not confined to the myocardium, 
but involves also the nervous mechanism; but the discoverable changes 
are inconspicuous. 

Symptoms. — Many persons, subjects of congenitally weak hearts, 
conscious perhaps of other cardiac deficiency, or readily made aware 
thereof upon slight exertion, lead a quiet and retired life — well within 
the functional capacity of their hearts — and suffer no noteworthy ill 
consequences. Others, however, endeavoring to attain the average of 
human activities, suffer upon slight or moderate exertion, with precordial 
distress or oppression, palpitation of the heart, rapid heart action (120 
or more per minute), with an unstable or irritable pulse, dyspnoea, general 
muscular weakness, etc. These symptoms may become of high grade 
and associated with more serious evidences of cardiac inadequacy 
should the patient lead an altogether ill-advised life, engage in athletic 
exercises, attempt feats of mountain climbing, etc. (consult the over- 
strained heart); or they may develop precipitously after some sudden 
severe exertion (consult acute dilatation of the heart). 

In the acquired cases the symptoms, as a rule, are analogous. In 
the postinfectious cases the patient during quietude does not suffer, 
but more or less distress, palpitation, and dyspnoea ensue upon activity, 
and the patient is generally weak. In the alcoholic and tobacco cases 
the patient may be conscious of palpitation, fluttering, or irregularity 
of the heart even when quiet, and dyspnoea develops upon exertion. 
These symptoms are often associated with other evidences of intoxica- 
tion, such as so-called indigestion, general nervousness, headache, and 
other mental symptoms. The disorder of the heart, of course, gradually 
passes over into well-recognized anatomical lesions (degenerative, chronic, 
fibrotic, etc.). 

In the anemic and cachectic cases, in addition to the general manifes- 
tations of anemia, there is more or less precordial distress, cardiac pal- 
pitation, rapid heart action, weak apex beat, feeble pulse, dyspnea, 
syncopal attacks, etc.; these are referable in part to the anemia as such, 
but they are due also in part to the weakened and usually dilated myo- 
cardium the result of insufficient nourishment. The condition gradually 
merges into parenchymatous and fatty degeneration and chronic dilata- 
tion of the heart. 

The neurotic cases are well exemplified in the more or less fleeting 
attacks that occur usually in neurotic women under most diverse circum- 



42G DISEASES OF THE MYOCARDIUM 

stances, and are manifested by sensations of stoppage of the heart or pre- 
ordial fluttering, pallor of the lips and face, and a general feeling of appre- 
hension, "sinking," impending syncope, or paresthetic phenomena; the 
pulse is usually weak and somewhat accelerated (not the pulse of syncope 
— which does not occur). The attack lasts a variable time, and may be 
followed by considerable exhaustion. In other cases, especially following 
a long period of mental overwork, worry, etc., the heart, sometimes 
quite suddenly, becomes weak and may necessitate the patient's taking 
to bed; in aggravated cases any position other than the prone leads to 
syncope, weak heart action, and feeble pulse. The apex beat is weak, 
the first sound is short and valvular, the second sound is rarely accen- 
tuated; the action of the heart is often irregular and readily disturbed in 
rate and rhythm by various influences. There are no hysterical symp- 
toms. Recovery may not ensue for several or many months. 

Diagnosis.— The diagnosis of the acquired cases is not difficult as 
a rule. The congenital cases often pass unnoticed, until at least more or 
less dilatation has ensued, whereupon the condition is scarcely to be 
distinguished from dilatation arising from other causes. In the early 
stages the history of the patient, the absence of etiological factors, the 
development of symptoms upon the slightest exertion and their aggra- 
vation upon exertion well borne by the average individual, and the 
absence of noteworthy physical signs, aside from the rapidity and overac- 
tion of the heart and smallness and frequency of the pulse, should serve 
for the recognition of the disorder. 

Prognosis. — In the congenital cases the outlook depends upon the 
mode of life of the patient, upon his living within the capabilities of 
his heart. The postinfectious cases usually eventuate in recovery, but 
this may be long delayed. The cases due to alcohol, tobacco, tea, 
coffee, etc., are likely to improve in the course of time, if the causative 
poison is discontinued and irreparable damage has not been done. 

Treatment. — The treatment is largely hygienic. In the congenital 
cases the patient should be well nourished and should be given tonics 
to improve the general blood condition and nutrition, and he should 
indulge in carefully regulated exercise under competent supervision 
with a view to strengthening his myocardium; considerable improvement 
often follows. The treatment of the postinfectious cases is similar; 
iron is often a very useful remedy, but rest to the disabled heart may 
be required for a long time. Digitalis, strychnine, and similar drugs 
often do harm; they may be required, in the event of failing cardiac 
compensation, but rapid or unstable action of the heart of itself is not 
an indication for their use. The cases due to alcohol, tobacco, and 
the like usually improve with discontinuance of the causative factor, 
but the bromides, valerian, and aconite often render material service 
in quieting the overactive heart. The transient disorders that occur 
in neurotic women demand little else than stimulation and other meas- 
ures useful in syncope; speaking generally, there is no danger in the 
attacks except that which lies in the habit of taking drams to cure or 



THE OVERSTRAINED OR IRRITABLE HEART 427 

prevent them (Allbutt). The more severe and prolonged neurotic eases 
are best treated by rest in bed, massage, hydrotherapy, nutritious food, 
strychnine, alcohol, iron, and arsenic. Later, benefit accrues from 
carefully regulated exercises. 



THE OVERSTRAINED OR IRRITABLE HEART. 

{Cardiac Strain; Muscular Strain of the Heart; The Soldier's Heart; 
The Athlete's Heart.) 

Etiology. — The term overstrained heart is used as a convenient 
designation of the condition that results from excessive muscular effort. 
Probably, however, the term might be employed to comprise in addition 
all the conditions of the heart in which the myocardium, relatively or 
absolutely, is at a disadvantage (functionally insufficient) in relation 
to the intracardiac and arterial pressure, and in which in consequence 
overstrain ensues; these comprise cases of chronic valvular disease, 
the fibroid heart, diseases of the coronary arteries, arteriosclerosis, etc., 
all of which are discussed under appropriate headings. Although it may 
be difficult to estimate the importance of strain in an individual case, 
inasmuch as it is often bound up with other etiological factors of cardio- 
vascular disease, such, as syphilis, alcoholism, gout, plumbism, renal 
disease, etc., its prime importance is manifest when we compare the 
heart disorders of men with those of women of the same station in life; 
and when we compare the heart disorders of men engaged in laborious 
occupations, such as draymen, ironworkers, blacksmiths, etc., with 
those of men not engaged in laborious occupations, but equally but not 
more given to the vices of intemperance and sexual immorality, such as 
clerks, business and professional men. In estimating the etiological 
significance of strain, one must take into consideration all of the factors 
in the individual case; and one may no more cursorily and without 
investigation attribute to strain certain manifest diseased conditions 
in a patient than he may elect to overlook the possible etiological impor- 
tance of a sudden and severe strain to which the patient himself may 
attribute the onset of his ailment. It is quite conceivable, indeed, it is 
quite true, that the healthy individual — the individual with his muscles, 
heart, bloodvessels, and lungs developed proportionately to the demands 
that he makes upon them — may endure a considerable amount of pro- 
longed or sudden strain without obvious ill consequences. This we 
observe almost every day in athletes and like persons. But we also 
observe very frequently the disastrous results to the heart and the 
general economy of sudden severe strain and of prolonged strain ill— 
advisedly persisted in, not only in a certain proportion of those engaged 
in athletic contests, but also in those whose occupation necessitates 
considerable strain, in those poorly endowed by nature, who soon use 
up their reserve strength, and in those with hearts weakened by typhoid 
fever, influenza, and other infections, anemic states, etc. 



428 DISEASES OF THE MYOCARDIUM 

Cardiac overstrain, in the restricted sense in which it is here employed, 
results: (1) From sudden violent muscular effort, such as may occur 
in lifting unusually heavyweights, in rowing races and similar contests, 
etc.; and (2) from repeated, long-continued, and ill-directed muscular 
exertion, such as may occur in college and other athletes, in all persons 
who engage unduly and inadvisedly in exercise, in soldiers subjected to 
forced and prolonged marches, etc. This overstrain of the heart, in 
view of the etiological factors, is largely a disorder of early adult life 
and of the male sex, but it is sometimes encountered in young women 
overzealous in the pursuit of athletics. It may develop in a heart pre- 
viously normal, as well as in a heart damaged by myocardial or valvular 
disease or weakened by general causes, such as fever states, anemia, etc. 

Pathology. — In sudden death from acute heart strain, all the chambers 
of the heart are dilated and filled with blood, and the lungs and the 
venous system are markedly engorged. In the chronic cases the heart 
shows more or less hypertrophy and dilatation, myocardial degeneration, 
perhaps mitral endocarditis, coronary arteriosclerosis, etc.; in a word, 
the more common concomitants of general and coronary arteriosclerosis. 

The chief causative factors of cardiac overstrain are increased arterial 
pressure and increased and accelerated flow of venous blood to the heart, 
both of which are provoked by muscular exertion. The increased arterial 
pressure occasions an insufficient and incomplete emptying of the 
left ventricle, which in turn leads to a gradually increasing residuum 
of blood within, and dilatation of, the ventricle; at the same time the 
increased and accelerated flow of venous blood leads to a similar condition 
of the right ventricle. Dilatation of the right ventricle is the more com- 
mon in the ordinary athletic contests, and can commonly be demonstrated 
by increased cardiac dulness to the right and a systolic murmur in the 
tricuspid region (tricuspid insufficiency; safety-valve action of the 
tricuspid valve). With cessation of the causative factor the heart, 
if previously healthy, reverts to its normal condition and no ill conse- 
quences ensue. Permanent damage, however, may follow the too 
frequent repetition of athletic contests or other muscular exertion, 
ill-directed athletic training, the non-adaptation of exercise to the indi- 
vidual — which is the essential etiological factor; this permanent damage 
occurs especially in young adults of poor physique, such as many college 
students, soldiers, etc. In the case of soldiers, to the other etiological 
factors one may add the weight of accoutrements, which embarrass 
respiration, the fatigue of prolonged marches, the abuse of tobacco 
and alcohol, venery, etc., all of which may gradually lead to what 
Da Costa so aptly described as the soldier's "irritable" heart. 

Symptoms. — A person subjected to severe muscular exertion in excess 
of the capabilities of his heart, complains of a sense of fulness, or dis- 
tress beneath the sternum and in the region of the heart, perhaps of 
actual pain that may radiate throughout the chest and into the arms; 
there is also palpitation of the heart, dyspnoea, general muscular weak- 
ness, vertigo, and sometimes even syncope. Observation discloses a 



THE OVERSTRAINED OR IRRITABLE HEART 429 

livid and anxious expression, with prominent eyes and dilated pupils, 
and excessive perspiration; fulness and pulsation of the veins of the neck; 
marked and widespread precordial pulsation; increased area of cardiac 
dulness especially to the right, with loud, clear, valvular heart sounds, 
a systolic murmur in the tricuspid area (relative tricuspid insufficiency; 
safety-valve action of the tricuspid valve), perhaps a systolic murmur 
elsewhere, and a weak pulse. These phenomena are to be interpreted 
as the manifestations of an acutely embarrassed heart. As a rule, espe- 
cially in previously healthy subjects, they subside and leave no ill con- 
sequences; in rare instances, especially in those the subjects of previous 
heart disease, they may lead to an immediately fatal issue; in other cases, 
the acute phenomena subside, but the patient finds himself in the 
future more or less incapacitated. The original distressing symptoms 
and embarrassed cardiac action are again provoked in the athlete by 
contests, such as football, basket ball, running, rowing, bicycling, etc.; 
in some cases even moderate exercise serves to bring on the symptoms; 
whereas, especially in older subjects with perhaps some myocardial de- 
generation, even the slightest exertion (climbing stairs or a hill), perhaps 
even a full meal, or too much tobacco or alcohol, or constipation with 
intestinal distention, leads to more or less distress (precordial distress, 
dyspnoea, palpitation of the heart, irregular or quickened heart action, 
etc.); that is, the heart is unusually sensitive to extraneous influences 
well borne by a normal heart: it is said to be irritable. Comparative 
comfort or freedom from distress may be secured by the patient's leading 
a quiet life and avoiding all muscular strain. The physical signs may be 
entirely normal, or there may be signs of hypertrophy with some dilata- 
tion of the heart. 

The more chronic cases, such as result from long continued excessive 
muscular exertion, present the common evidences of increased arterial 
pressure and hypertrophy of the heart, together with a marked tendency 
to the occurrence, upon exertion, of the aforementioned signs of cardiac 
embarrassment. The physical signs are those of hypertrophy and dilata- 
tion of the heart, of which the one or the other may predominate in the 
individual case. 

Diagnosis.— In the acute cases the history and the mode of life of the 
individual are of great importance in determining the cause of the 
symptoms, especially in cases in which the physical signs are equivocal. 
The effect of exertion purposely undertaken under the observation of 
the physician may be of service in establishing a diagnosis. In the 
chronic cases the diagnosis depends upon a history of long continued 
overexertion and the physical signs of heightened blood pressure and 
dilated hypertrophy of the heart. 

Prognosis. — In the acute cases the outlook depends entirely upon the 
future life of the individual, upon his avoiding the causes known to pro- 
voke cardiac distress. The prognosis in the chronic cases is that of 
hypertrophy and dilatation of the heart. 






430 DISEASES OF THE MYOCARDIUM 

Treatment. — Overstrain of the heart should be prevented — by thorough 
physical examination of the heart of all intending athletes, soldiers, etc., 
by the avoiding of muscular exertion obviously too severe for the sub- 
ject, and by proper training under supervision. By graduated exercises 
a weak but otherwise normal heart may be made stronger, and capable 
of sustaining greater efforts. Sudden severe overstraining of the heart 
often leads to more or less irreparable damage to the heart. The acute 
symptoms are best met by rest in the recumbent posture and diffusible 
stimulants, such as whiskey, brandy, aromatic spirit of ammonia, 
compound spirit of ether, etc.; in rare cases bleeding may be required. 
After recovery from these acute symptoms, rest for a long time is impera- 
tive. The patient must avoid all factors that in the least tend to irritate 
or accelerate the heart: not only exercise, but also alcohol, tobacco, 
tea, coffee, etc. After the lapse of several months graduated exercise, 
most carefully supervised, is often of service. The overacting, irritable 
heart may often be quieted by the use of the bromides, valerian, aconite, 
etc. Cardiac tonics, such as digitalis, strychnine, etc., are of little service, 
except in the more chronic cases with dilatation, the treatment of which 
is that of failing cardiac compensation in general. 



THE FATTY HEART. 

Etiology. — The term fatty heart is applied to two conditions, fatty 
degeneration and fatty infiltration. Although they may occur together, 
in well-marked cases, they represent two quite distinct diseases. Fatty 
degeneration usually follows and is associated with parenchymatous 
degeneration, and is due, therefore, to like causes; but it occurs also in 
many forms of hypertrophy, in old age, etc. Fatty infiltration or over- 
growth is an excess of the normal subpericardial fat, and is a part of 
general obesity. 

Pathology. — Usually the fatty deposit is most marked along the 
course of the larger coronary vessels and in the auriculoventricular 
furrows; but it may entirely envelop the heart in a thick casing and may 
infiltrate between the muscular fibers even to the endocardium. In some 
regions the muscular fibers may be entirely replaced by the fatty tissue. 
Aside from the fatty deposit, the heart may be quite normal, but it is 
usually somewhat enlarged, hypertrophied in consequence of excessive 
food and drink, and dilated in consequence of muscular weakness. 
In addition to the fatty deposit there is usually some fatty degeneration 
and simple and brown atrophy of the muscular fibers; the coronary 
arteries often reveal some sclerosis, and there are consecutive areas of 
fibrosis of the myocardium. 

It is difficult in many cases to determine to what degree the symptoms 
are due to the fatty deposit. It is not improbable that a large encasement 
of fat more or less seriously compromises the functional activity of the 
heart, but there are many cases of well-marked fatty infiltration of the 



THE INFECTIOUS FEBRILE HEART 431 

heart that present no symptoms until the advent of dilatation, and many 
fatty hearts with symptoms reveal in addition coronary sclerosis and 
fibroid myocardium — which may well be answerable for the symptoms. 
Perhaps in many cases the fatty deposit is secondary to primary atrophy 
of the muscular fibers. 

Symptoms. — The majority of obese subjects sooner or later complain 
of dyspnoea, slight cyanosis, and palpitation of the heart on exertion 
(these are often due, in part at least, to the obesity itself and interference 
with the action of the muscles of respiration); others have periodical 
attacks of so-called asthma (perhaps induced by overeating or over- 
drinking), or of bronchitis; still others complain of vertigo, pseudo- 
apoplectic attacks, with Cheyne-Stokes breathing, anginoid pains, or 
angina pectoris. Examination of the heart (rendered difficult by the 
excessive panniculus adiposus) reveals increase in the area of cardiac 
dulness and weak or muffled cardiac sounds; and the pulse is small and 
weak. In the course of time, unless properly and efficiently treated, 
the symptoms of failing compensation (dyspnoea, passive congestion of 
the viscera, and oedema), with a murmur of relative mitral, and perhaps 
tricuspid, insufficiency, may develop; or the patient may die suddenly 
in an anginoid attack. 

Diagnosis. — The diagnosis, which rests upon cardiac enfeeblement 
in an obese subject, is always precarious; the symptoms doubtless 
are often due less to the fat about the heart than to associated lesions. 

Prognosis . — The prognosis virtually is that of obesity plus the asso- 
ciated cardiac conditions. 

Treatment. — The treatment is that of obesity, associated with appro- 
priate measures to invigorate the action of the heart. The so-called 
Oertel treatment (regulated diet, largely protein, limitation of the fluid 
intake, and graduated exercises up hill) here finds an especial field of 
utility. 

THE INFECTIOUS FEBRILE HEART. 

{Myocardial Degeneration; Parenchymatous and Fatty Degeneration of the Heart; 

Acute Myocarditis.) 

The infectious febrile heart is a somewhat inapt and perhaps ill-chosen 
term designed to describe the condition of the heart in the acute infec- 
tious processes; the lesions are chiefly degenerative, but to these in some 
cases inflammatory changes are added. 

Etiology. — The etiological factors are the toxins of the acute infections 
generally, but notably, acute rheumatic fever, typhoid fever, pneumo- 
coccic and other pyococcic infections (septicopyemias), influenza, 
diphtheria, etc. These toxins perhaps act upon the nervous mechanism, 
stimulating the accelerator nerves, since fever of itself is accompanied 
by an accelerated heart-rate. The chief influence of the toxins, however, 
is exerted on the myocardium and the vasomotor system. 






432 DISEASES OF THE MYOCARDIUM 

Pathology. — The changes vary considerably in different cases. In some 
they are slight and apparently inconsequential, transitory in nature, 
and leave no permanent ill consequences. In others there is a varying 
reaction of the myocardium to the toxin; whereas in still others there 
may be also endocarditis or pericarditis, or what may be properly spoken 
of as carditis or pancarditis. Endocarditis and pericarditis are described 
elsewhere, but it is perhaps wise to point out here that most of the 
symptoms and signs of these disorders, such as precordial distress, 
dyspnoea, cardiac and pulse irregularities, changes in the size of the 
cardiac dulness, as well as some murmurs, etc., are of myocardial origin. 

At the necropsy, after a fatality in one of the aforementioned acute 
infections, the myocardium, to the unaided eye, is usually pale and opaque, 
and flabby or friable; occasionally it is streaked with yellowish lines, 
especially that of the left ventricle and the papillary muscles. The heart 
may be more or less dilated; the cavities may be filled with laminated 
and anemic clots; but sometimes in sudden death they are quite empty 
(vasomotor collapse). Microscopically the muscle fibers are swollen 
and opaque, the seat of more or less advanced albuminous, granular, 
or parenchymatous degeneration (cloudy swelling). The lesions, if 
unchecked, proceed to fatty degeneration (the yellowish streaks in the 
muscle of the ventricles or the papillary muscles); or there may be asso- 
ciated hyaline or amyloid degeneration. The nerves may reveal degenera- 
tive changes. The interstitial tissue often reveals little if any change. 
In some cases, especially of severe infections, or associated with endo- 
carditis or pericarditis, there is, in addition to the myocardial degen- 
eration, more or less vascular dilatation and cellular exudation and 
proliferation (acute interstitial myocarditis). The lesions may subside 
or give rise to a form of chronic myocarditis. In septicopyemia there 
may be embolism of the small coronary vessels, with scattered foci of 
suppuration containing the causative microorganisms (suppurative 
myocarditis). In favorable cases the small abscesses become inspissated 
and a cicatrix ultimately forms, leading to a form of chronic localized 
myocarditis, with perhaps the later development of an aneurysm of the 
heart; in other cases the abscess may increase in size and ultimately 
rupture into the pericardium or a cavity of the heart. 

Symptoms. — From the nature of the etiological factors cardiac symp- 
toms are often in abeyance, being masked by those of the primary 
disorder. In many of the infections there may be no complaint whatever 
while the patient is at rest in bed; dyspnoea and palpitation of the heart, 
however, not infrequently follow even slight exertions, and excitability of 
the heart is shown in attacks of rapid, irregular, and intermittent action 
upon slight " starts," emotional and other disturbances, etc. (toxic depres- 
sion of conductivity and the dropping out of ventricular systoles). In 
other cases the pulse is persistently rapid. In the majority of infectious 
or toxic cases the symptoms develop as the patient, convalescing, begins 
to substitute the activity of returning health for the prone and quiet 
posture of disease. The first symptom may be a sudden and fatal 



THE INFECTIOUS FEBRILE HEART 433 

attack of heart or vasomotor failure, such as not infrequently occurs 
during convalescence from diphtheria. In other cases less severe 
attacks of heart failure occur; syncope attends the upright posture 
or the getting out of bed; in other cases the heart becomes rapid, and is 
subject to periods of irregularity and intermittency on exertion or 
excitement. But in a notable series of cases the patient presents general 
evidence of cardiac inadequacy (depression of tonicity) ; he complains of 
muscular lassitude and of cold hands and feet and nose; while generally 
pallid, his toes and finger tips and nose and ears may be bluish (capillary 
stasis); he is mentally torpid and does not respond to mental or other 
stimuli; the urine is of low specific gravity, reduced in amount, and may 
contain a slight trace of albumin; and there may be vomiting. In many 
of these cases, to the cardiac inadequacy vasomotor failure is added; 
this may readily be determined by a rapid pulse and low blood pressure. 
Systolic pressures of 100 mm. Hg. are not uncommon; less than 80 mm. 
may be found in severe infections, and is of serious moment. In unusual 
cases, instead of rapidity there may be unusual slowness of the heart 
action, proceeding even to heart block. Influenza sometimes attacks 
the heart with special severity. During the attack there may be marked 
prostration, with dyspnoea, cardiac palpitation, syncope, and very 
feeble heart sounds; after the attack has subsided dyspnoea and tachy- 
cardia often persist, and may be associated with precordial pain and 
distress or anginoid pains on exertion. 

Examination reveals the heart action rapid, irregular, or intermittent; 
usually but not always there is some dilatation; the apex beat is weak 
and diffuse; the first sound at the apex is muffled and prolonged, or weak, 
short, and valvular; or it may be replaced by a variable blowing systolic 
murmur (relative mitral insufficiency from stretching of the mitral ring, 
or from irregular or incoordinated action of the papillary muscles); the 
pulmonary second sound is usually accentuated; and the blood pressure, 
as a rule, is low (often less than 100 mm. Hg.), but fluctuates much from 
time to time and is unusually responsive to divers sorts of extraneous influ- 
ences. Added sounds (extrasystoles) may be audible. The heart may 
also be observed to dilate under exertion or excitement. 

Diagnosis. — The diagnosis should be apparent from the etiological 
factors and the obvious evidences of weak, irritable, or unstable cardiac 
action, especially a rapid, irregular, and feeble, or a very feeble, slow 
pulse, capillary stasis, weak apex beat, weak and valvular first sound 
of the heart, evidences of dilatation, variable apex murmur, and low 
blood pressure. 

Prognosis. — As a rule, most cases eventuate in recovery with the cure 
of the initiating disorder; but, as in the influenzal and other cases, this 
may be longer delayed. Occasionally the heart remains for a long time 
or permanently susceptible, and dyspnoea and palpitation develop on 
slight provocation. 

Treatment. Attempts should be made to minimize the damage to the 
heart by the use of antitoxin in diphtheria; by hydrotherapeutic measures 
28 



434 DISEASES OF THE MYOCARDIUM 

to reduce the fever, especially in cases of long continued or high fever; 
and by free elimination in all toxic conditions. Absolute rest in bed is 
the most important element of the treatment; it should be prolonged 
especially in diphtheria, scarlatina, severe pneumonia, influenza, etc., 
and the getting up and about should be gradual and controlled by the 
effect on the heart and the pulse. Especial attention should be paid to the 
diet, which should be wholesome, highly nutritious, and readily digestible. 
Iron, quinine, the bitter tonics, and alcohol are the most suitable remedies; 
these may be augmented by cold affusions and other simple hydrothera- 
peutic measures, which are of the utmost value in restoring tone to the 
cardiac muscle and the vasomotor system. Cardiac tonics, such as digi- 
talis, strophanthus, strychnine (except in very small doses), are contra- 
indicated, in the early stages at least. In protracted, slowly progressing 
cases, small doses of digitalis often prove serviceable. In these cases 
also massage and graduated exercises are of value. 

Attacks of acute failure of the heart are to be met with diffusible 
stimulants, such as aromatic spirit of ammonia, compound spirit of 
ether, brandy, whiskey, hot coffee, etc., by the mouth; or whiskey, 
caffeine, camphor in oil, strophantin, adrenalin chloride, etc., hypo- 
dermicly, with adrenalin chloride and physiological saline solution 
by the bowel, hypodermically, or intravenously. The acute failure 
with marked dilatation of the heart is sometimes promptly relieved by 
venesection. 

THE FIBROID HEART. 

(Chronic Interstitial Myocarditis; Fibroid Degeneration of the Myocardium; 
Sclerosis of the Coronary Arteries.) 

Etiology. — In the great majority of cases the fibroid heart is a result 
of sclerosis of the coronary arteries, which in turn may be a more or less 
independent disorder, but usually is merely part of general arteriosclerosis ; 
the causes of the one, therefore, are the causes of the other, notably 
alcoholism, syphilis, habitual and excessive muscular work; but, as in 
arteriosclerosis generally, excessive eating, gout, prolonged and exces- 
sive mental efforts, lead poisoning, etc., also are of significance. The 
disorder, therefore, is more common in the male sex and after the 
fortieth year; and in some cases it seems to be predisposed to by heredi- 
tary influences. Occasionally chronic myocarditis results from or is a 
sequel of acute myocarditis, representing the healing and cicatrization 
of the acute lesions; or it is associated with endocarditis and pericarditis, 
representing an extension into the myocardium of the lesions of either 
of these two disorders; or it is intimately bound up with the conditions 
of hypertrophy and dilatation, and of the so-called fatty heart. Finally, 
the disorder may be merely an expression of advancing age. 

Pathology. — The lesions may be diffused or circumscribed. The 
circumscribed lesions implicate especially the left ventricle, more par- 
ticularly the apex, and less frequently the septum, the right ventricle, 



THE FIBROID HEART 435 

the papillary muscles, and the auricles. They consist of firm, whitish 
streaks or patches, of variable size, interspersed between the muscular 
fibers. Usually these areas can be demonstrated to be directly related 
to sclerotic changes in the finer branches of the coronary arteries. In 
consequence of lessening of the lumen of these small vessels (obliterating 
endarteritis) the portion of myocardium thereby supplied with blood 
becomes imperfectly nourished, gradually undergoes degenerative and 
atrophic changes, and is ultimately replaced by connective tissue. 
Occasionally the interruption in the arterial supply is sudden (thrombosis 
or embolism), and if the patient does not die immediately, an area of 
anemic or hemorrhagic infarction ensues and is usually replaced by a 
scar. Associated with the fibrosis there is more or less hypertrophy and 
dilatation, varying in grade in different parts of the heart. Since a heart 
ill supplied with blood cannot hypertrophy, the hypertrophy must be 
due to extracardiac factors, notably an antecedent valvular disease, 
general arteriosclerosis, chronic nephritis, idiopathic hypertrophy, or 
localized hypertrophy of the non-involved portion of the myocardium, 
etc.; the dilatation is the result of the gradual yielding of a weakened 
myocardium to the intracardiac pressure. Sometimes the yielding 
is limited to, or marked at, a small area (scar of a healed infarct), and a 
so-called cardiac aneurysm results; exceptionally this or the initial area 
of infarction may rupture and give rise to sudden death. In those cases 
in which there is extensive fatty change, the sclerosis has usually involved 
the larger branches of the coronary arteries rather than the smaller 
twigs, and leads to a general interference with the nutrition of the 
myocardium. 

Symptoms. — The symptoms are extremely variable. In some cases 
there are no noteworthy symptoms whatever, more or less extensive 
myocardial fibrosis being found after death from other causes. In these 
cases, of course, the demands made upon the myocardium were still 
within the limit of its capabilities. Symptoms when they develop are 
those of embarrassed or insufficient heart action, developing, as a rule, 
gradually in a man past middle life. Sometimes the symptoms are 
precipitated by an intercurrent disorder, such as pneumonia or other 
infection, or by some intoxication, such as an alcoholic debauch or an 
attack of acute gout, or by some unusual exertion or excitement precipi- 
tating dilatation of the heart. In the cases beginning thus, more or 
less suddenly, the symptoms are those of more or less well-marked 
cardiac decompensation. In the cases of more gradual development 
the patient begins to notice general sallowness of the integument, weak- 
ness, and languor; he is readily tired, and less capable than formerly 
of mental or physical exertion: the first induces fatigue and mental 
depression, and the second dyspnoea, palpitation of the heart, precordial 
distress, and perhaps syncopal attacks (cerebral anemia). With increas- 
ing dilatation of the heart, the phenomena of failing compensation 
(cyanosis, oedema, passive congestion of the viscera, etc.) develop. 
Another series of cases is characterized by anginoid pains or attacks 



436 DISEASES OF THE MYOCARDIUM 

of true angina pectoris. In another series of cases the phenomena of the 
Stokes-Adams syndrome develop; or a person apparently in good health 
dies suddenly (coronary thrombosis and anemic infarcts, fatty degenera- 
tion of the heart, or extensive fibrosis) ; or the symptoms may be merely 
those of advancing age. 

Examination of the heart reveals variations in accordance with asso- 
ciated conditions, arteriosclerosis, chronic nephritis, valvular disease, 
chronic pericarditis, emphysema, etc. Usually there is more or less 
hypertrophy with dilatation. The apex beat is displaced downward 
and outward in accordance with the predominating hypertrophy and 
dilatation, and it is feeble; often, indeed, it is entirely absent. The 
first sound of the heart varies: it may be feeble or muffled, suggesting 
irregularity of the muscular contractions; or it may be loud and valvular 
(disproportionately loud as compared with the feeble apex beat) suggesting 
more or less complete loss of the muscular element ; or, and this is quite 
significant, there may be a distinct gallop rhythm. This may be of the pre- 
systolic type, in which the new third sound immediately precedes the normal 
first sound of the heart, and is due to a strongly acting hypertrophied 
auricle, or, if heard in weak and rapidly acting hearts, is due to a delay 
in conductivity and sufficient separation in time of the auricular and 
the ventricular contractions to enable one to differentiate the separate 
sounds produced by both; or the gallop rhythm may be of the proto- 
diastolic type, in which the new third sound occurs in the early part 
of diastole immediately following the normal second sound, or it may 
be mesodiastolic, in which the new sound occurs in the middle of diastole; 
in both of these the new sound is ventricular in origin and is perhaps 
due to loss of tonicity of the ventricular muscle and its sudden dis- 
tention by an ample and rapid volume of blood. The second sound 
may be reduplicated, but this is less frequent than in valvular disease. 
There are commonly no murmurs until the disease is fairly well ad- 
vanced, when a systolic murmur of relative mitral insufficiency and per- 
haps also of tricuspid insufficiency, may ensue, the consequence of inco- 
ordination of the papillary muscle or dilatation of the arterioventricular 
rings. The cardiac action and the pulse are often irregular in rhythm 
and force; the pulse is usually small and feeble; it may be rapid, but 
it is often characteristically slow, 60, 50, or less to the minute, and not 
uncommonly exhibits extrasystoles (pulsus bigeminus). 

Diagnosis. — The diagnosis is often difficult and sometimes impossible, 
but special significance attaches to the manifestation of a failing or 
embarrassed heart in a middle-aged person without the etiological 
factors and concomitant signs of valvular disease; and especially to a 
slow, irregular pulse, attacks of anginoid pains or syncope, and evidences 
of sclerosis of the palpable arteries. 

Prognosis. — The prognosis is always grave, since restitution to the 
normal is impossible; but with care and the adoption of a suitable mode 
of life the patient may live many years. 



HYPERTROPHY AND DILATATION OF THE HEART 437 

Treatment. — In the cases of gradual onset and slow progress, as well 
as in the heart of fatty overgrowth, much can often be done to arrest 
the progress of the disorder by regulation of the mode of life, especially 
as regards eating and drinking, and by properly regulated rest and 
exercise. The so-called Oertel cure (regulated diet, largely protein, 
limitation of the fluid intake, and graduated exercises up hill) and the 
Schott or Nauheim treatment (effervescing baths and resisted exercises) 
are often very advantageous. Cases developed upon a syphilitic basis 
may perhaps be benefited by the use of the iodides, which also may be 
given in any case of arteriosclerosis; benefit sometimes attends its 
prolonged use. Cases of obvious cardiac insufficiency, manifested by 
dyspnoea, cyanosis, oedema, and rapid and irregular pulse, etc., are to 
be treated as is the decompensation of valvular disease. The cases with 
slow pulse and no signs of dilatation are to be treated with diffusible 
and other stimulants, and with morphine (in the event of restlessness, 
nervousness, anxiety, etc.), and nitroglycerin (in the event of high blood 
pressure); digitalis is contra-indicated. 



HYPERTROPHY AND DILATATION OF THE HEART. 

(Enlargement of the Heart.) 

Enlargement of the heart may be due to hypertrophy, to dilatation, 
or to both. By simple hypertrophy is meant a simple increase in the 
thickness of the muscular walls without increase in the size (or capacity) 
of the heart cavities; by eccentric hypertrophy is meant increase in the 
thickness of the muscular walls with increase in the capacity of the 
cavities. Increase in the thickness of the walls with diminution in the 
size of the cavities probably never occurs (formerly so-called eccentric 
hypertrophy). 

Etiology. — Hypertrophy and dilatation, although often the obtrusive 
evidence of disorder of the heart, are, in the great majority of cases, the 
expression of the activity of more or less remote causative factors. In 
most cases the hypertrophy and dilatation, which are usually combined, 
are readily referred to a manifest valvular defect; but occurring inde- 
pendently of valvular disease, the hypertrophy or dilatation is frequently 
overlooked, or, being detected, is set down as a primary disorder, when 
in reality it is a result or part and parcel of other diseased conditions. 

In general, hypertrophy or dilatation is an expression of the functional 
capacity of, and of the demands made upon, the heart; it represents the 
relationship between the power possessed by the heart and the work that 
it is called upon to perform. In health there is a balance between 
these, and, to the astonishment of all who think of it, the heart that 
never ceases its activity remains normal. When, upon occasion, the heart 
is called upon temporarily to perform some unusual work, its reserve 
force is such that it is usually enabled to do it without damage to itself. 
Such, however, mav be the inherent weakness of the heart, or the dis- 



438 DISEASES OF THE MYOCARDIUM 

proportionately great amount of work that it is called upon to perform, 
that it succumbs (cardiac overstrain), and acute dilatation results. 
On the other hand, the increased amount of work may be moderate 
in amount but frequently repeated, in which circumstance the heart 
fortifies itself by hypertrophy — in many respects a conservative process. 
In this manner the heart is enabled to perform the increased amount of 
work for some time — until its nutrition suffers or the work becomes 
too great, whereupon dilatation and the usual evidences of embarrassed 
circulation, of failing cardiac compensation, result. Thus, dilatation, 
both acute and chronic, not infrequently occurs without associated 
hypertrophy; but whether hypertrophy ever occurs independently of 
dilatation may well be doubted — most if not all cases of so-called con- 
centric hypertrophy reported being examples of postmortem contrac- 
tion of the heart. 

Hypertrophy and dilatation may affect the heart as a whole, or may be 
confined to one side or to one of the four great divisions of the organ. 
Usually there is associated disease of both sides, and not uncommonly 
of all four divisions. The hypertrophy and dilatation of valvular disease 
is discussed under the appropriate headings; occurring independently 
of valvular disease, there are the following clinical varieties: (1) Acute 
dilatation; (2) chronic dilatation; and (3) hypertrophy, or, as it is 
sometimes called, dilated hypertrophy. 

Acute Dilatation. — Acute dilatation is a common event in the course 
of many of the acute infective diseases, and not infrequently leads to 
death (see the infectious febrile heart). Acute dilatation may be 
observed also in certain chronic diseased states, such as are attended by 
grave secondary anemia and degenerative alterations of the myocardium. 
In some of these cases the heart, gradually failing, may suddenly dilate, 
although chronic dilatation is the more common event. Acute dilatation 
results also from sudden violent exertions — from the attempting of work 
altogether disproportionate to the natural and reserve force of the heart. 
Thus, we find it in draymen and ironworkers who suddenly exert all their 
muscular power in the effort to lift heavy weights; in athletes, oarsmen, 
runners, football players, etc., after participation in some unduly stren- 
uous contest; in mountain climbers, especially in those who attempt 
difficult ascents to which they are unaccustomed, etc. It is a feature also 
of what is known as angiospastic dilatation of the heart. 

Chronic Dilatation. — Chronic dilatation, occurring independently 
of valvular disease, is common in states of general malnutrition attended 
by grave secondary anemia. It attends fatty degeneration of the heart 
muscle, myocarditis, fibroid heart, and pericardial adhesions. It is a 
terminal event in hypertrophy from whatever cause arisen, unless the 
subject dies of an intercurrent affection. It results from gradual weak- 
ness (loss of tonicity) of the heart muscle, which becomes less and less 
able to perform its allotted work. 

Hypertrophy. — Hypertrophy of the heart, occurring independently 
of valvular disease, may be due to a variety of causes. The hypertrophy 



HYPERTROPHY AND DILATATION OF THE HEART 439 

that effects especially the right ventricle is due to increased pressure in 
the pulmonary circulation, and is found most commonly associated 
with emphysema, fibroid lung, chronic bronchitis, chronic pleural 
adhesions with contraction, etc. It is really a part of these diseases — a 
conservative process on the part of the heart, a condition that arises 
in response to increased demands upon the heart. It may persist for 
years, enabling the heart to do the increased work well, and the patient 
may die of an entirely independent affection. In many cases, however, 
dilatation and its attendant phenomena ultimately result. 

Hypertrophy of the left ventricle, occurring independently of valvular 
disease, results from increased pressure in the systemic circulation, and 
from increased activity of the heart. Among the rarer causes are con- 
genital hypoplasia of the aorta, such as is sometimes observed in chlorosis 
and other conditions; narrowing of the aorta, usually congenital and 
occurring in the neighborhood of the ductus Botalli; aneurysm of the aorta, 
usually, however, associated with general arteriosclerosis or aortic valve 
disease; pressure on and obstruction of the aorta, such as may be ob- 
served in intrathoracic tumor and indurative mediastino-pericarditis, etc. 
Practically, however, in the majority of cases, hypertrophy of the left 
ventricle partakes of one of three varieties: (1) That due to arterio- 
sclerosis ; (2) that due to renal disease ; and (3) that, for want of a better 
name, known as idiopathic hypertrophy of the heart. In some cases it 
is difficult to refer the hypertrophy to one or the other of these classes, 
inasmuch as two or three may be concerned in the causation of the 
hypertrophy in the individual case. Thus, arteriosclerosis and renal 
disease are frequently associated, and the subject of one or both of these 
is frequently exposed to the causative factors of the so-called idiopathic 
hypertrophy. 

The hypertrophy of arteriosclerosis is common in advanced life — when 
to a considerable extent it is a conservative process. But it occurs fre- 
quently enough in relatively early life, when it is bound up etiologically 
with syphilis, alcoholism, plumbism, rheumatism, gout, etc. In the early 
stages the hypertrophied and contracted arterioles oppose a barrier to 
the onward movement of the blood, and high tension results. To over- 
come these, the heart, reacting to the stimulus of increased work, hyper- 
trophies. Later the arteries become rigid and more or less incapable of 
contracting. Thus, an important adjunct to the onward movement of 
the blood — the activity of the arteries themselves — is lost, and the heart 
must compensate by hypertrophy. Ultimately the entire arterial system 
may become extremely rigid and permanently distended, whereupon the 
heart must furnish almost if not quite all the poAver for the movement 
of the blood, and this is possible only through marked hypertrophy. 
At the same time, the coronary arteries participate in the process, the 
nutrition of the heart does not keep pace with its increase in size, and 
chronic dilatation ensues. 

The hypertrophy of the heart of renal disease occurs in all types but 
not in all cases of nephritis; it is most common and most marked in 



440 DISEASES OF THE MYOCARDIUM 

chronic diffuse indurative (or interstitial) nephritis, in which it is 
properly looked upon as part and parcel of widespread disease of the 
cardiovascular and renal systems. In the majority of cases the disorder 
doubtless commences in the kidneys, but it speedily implicates the heart 
and the blood vessels; in some cases the lesions begin simultaneously in 
the kidneys and in the cardiovascular apparatus. The primary factor 
is always increased blood pressure, which is discussed in detail under 
nephritis 

Idiopathic Hypertrophy of the Heart. — In a certain proportion of 
cases of cardiac hypertrophy (usually associated with some dilatation) 
none of the ordinary causes can be determined upon. There is neither 
valvular disease nor disease of the coronary or systemic arteries; no 
disorder of the myocardium as such, no pulmonary emphysema or other 
disease of the lung, no chronic nephritis, no arteriosclerosis, and yet there 
is cardiac hypertrophy. Eliminating the other and rarer causative 
factors previously mentioned, these cases — for want of a better term — 
are known as cases of idiopathic hypertrophy of the heart. 

Some at least of these cases are due to nervous causes, to persistent 
overactivity of the heart induced by undue irritability or overstimulation 
of the nervous mechanism. This is sometimes seen in nervous persons, 
in those susceptible and unduly exposed to psychic disturbances; it is 
found also in some cases of exophthalmic goitre; and is sometimes 
due to the misuse of tea, coffee, tobacco, etc. 

Another class of cases is undoubtedly due to excessive eating and 
drinking. There can be little doubt that excessive eating temporarily 
increases the specific gravity of the blood, and excessive drinking the 
total volume of the blood; these, together with the stimulating effect of 
certain metabolic products, result in increasing temporarily the blood 
pressure and the frequency and quickness of the heart's action. The 
frequent repetition of this calls for more work on the part of the heart, 
and when its reserve force has been exhausted hypertrophy ensues. 
This is seen well exemplified in the great hypertrophy of the heart in 
beer drinkers (the Munich beer-heart), and in the obesity of indulgence, 
especially in men over forty years of age. Alcohol in these cases is 
probably a contributing factor, but it is probably less answerable for 
the hypertrophy (which, as already mentioned, is to a certain extent a 
conservative process) than it is for arterial alterations and subsequent 
degenerative changes in the heart. 

Finally, one of the most interesting causes of cardiac hypertrophy 
is excessive muscular strain (which has been discussed under the over- 
strained heart). 

Pathology. — The conspicuous alterations are increase in the size of 
the heart, increase in the thickness of the walls, and change in the shape. 
The normal heart weighs from 250 grams (woman) to 300 grams (man); 
in hypertrophy with dilatation the weight is often twice or thrice this, 
sometimes more. In health the left ventricle measures 8 to 14 mm. 
in thickness, the right 4 to 7 mm., the left auricle 2 to 3 mm., and the 






HYPERTROPHY AND DILATATION OF THE HEART 441 

right auricle 1 to 2 mm. When diseased, the left ventricle may measure 
20 to 25 mm., the right ventricle 8 to 15 mm., the left auricle 3 to 4 mm., 
the right auricle 2 to 3 mm. The papillary muscles share in the hyper- 
trophy. When there is marked dilatation, thinning of the walls is often 
more apparent than real, being relative only. The cavities of the heart 
are greatly increased in capacity, being doubled, or even tripled; such 
may be the distention that relative insufficiency of otherwise normal 
valves ensues. The heart is variously altered in shape, depending upon 
the portion of the heart especially affected. In general, the apex becomes 
broader and blunter; this is especially the case in hypertrophy of the right 
ventricle, in which the heart as a whole becomes globular, and the entire 
apex may be made up of the thickened right ventricle; in hypertrophy 
of the left ventricle, although the apex is broader than normally, the heart 
still preserves its conical shape. When dilatation supervenes the heart 
becomes generally rounded. In the early stages of hypertrophy the 
heart muscle is firm to the touch, and dark red brown in color; in increas- 
ing dilatation, however, it loses its firmness, and becomes flaccid, and in 
high degrees of dilatation it is commonly a misshapen, toneless mass 
of tissue at the necropsy. Microscopically there is an increase in the 
number and size of the muscular fibers; in late stages fatty degeneration 
of the myocordium and fibroid alterations ensue. 

Symptoms. — Hypertrophy of the heart, since it is a conservative 
process on the part of nature, frequently exists for a considerable time 
without occasioning symptoms; indeed, by its presence it obviates 
certain symptoms that otherwise would develop on account of the 
diseased condition which it endeavors to correct. Sometimes, however, 
there are unpleasant sensations in the region of the heart, evidences 
of overactivity of the heart, precordial distress, rarely amounting to 
pain, subjective appreciation of the heart's action, etc. These are 
especially noticeable after exertion or excitement, when they may be 
accompanied by slight dyspnoea, vertigo, etc. Sooner or later, however, 
there are symptoms. These, in large part, are not to be distinguished 
from those of failing cardiac compensation occurring in the course of 
myocarditis or chronic endocarditis. The early symptoms in such cases, 
however, differ. Thus, in athletes and others whose hypertrophy is due 
to excessive muscular exercise, and who rather suddenly cease this 
muscular activity, there may be the subjective manifestations of over- 
activity of the heart, precordial distress, dyspnoea, cough, hemoptysis, 
tinnitus aurium, vertigo, flushings, disturbed vision, etc. (consult 
the overstrained heart). In other cases more or less constant and 
persistent dyspnoea precedes the final breakdown. 

The symptoms of acute dilatation are those already mentioned under 
acute cardiac overstrain and under the infectious febrile heart. The 
symptoms of chronic dilatation are those of decompensation, described 
under chronic valvular disease of the heart — precordial distress and 
pain, cough, dyspnoea, cyanosis, oedema, congestion of the viscera, etc. 



442 DISEASES OF THE MYOCARDIUM 

Physical Signs. — The physical signs vary somewhat, depending upon 
the portion of the heart affected. 

Left Ventricle. — Inspection and palpitation reveal bulging of the 
precordium, which in young subjects may cause marked asymmetry 
of the chest, widening of the intercostal spaces, increase in the force 
of the apex beat, and a widely diffused heart beat. The apex beat 
may be as low as the sixth, seventh, or eighth intercostal space, and 
2 to 5 cm. outside the mid-clavicular nipple line (13 to 18 cm. from the 
median line). The apex beat is peculiarly deliberate and heaving in 
character, increased in strength, and about 2 fingers' breadths in width. 
In some cases of well-marked hypertrophy a double apex beat may be 
felt, the second being attributed to a rebound of the heart transmitted 
from the aortic valve. Percussion reveals an increase in the area of 
dulness, which is more ovoid than in health, the long axis of the ovoid 
being directed in the long axis of the heart. The dull area (deep or 
relative dulness) may extend upward to the third rib, rarely to the second 
interspace, to the left 2 to 5 cm. beyond the mid-clavicular line, while 
to the right, in uncomplicated hypertrophy of the left ventricle, the 
increase of dulness is relatively slight — not more than 2 cm. (f inch) beyond 
the right edge of the sternum. On auscultation, if the valves are still 
competent, the heart sounds are normal, or the first sound is dull, some- 
what louder, and more prolonged than normally (due to increase of 
the muscular element). The aortic second sound is usually accentuated, 
sometimes reduplicated or split. The pulse is regular, of good volume, 
increased in strength and in tension. 

Right Ventricle. — Inspection and palpation reveal bulging of the 
precordium, especially at the xyphoid cartilage and adjacent right 
cartilages, with some widening of the intercostal spaces. The heart-beat 
is diffuse — the strongest beat not infrequently being at the lower part 
of the sternum. The apex beat also is diffuse, wider than normally — 
2 to 3 fingers' breadths in width — and extends to the left beyond the 
mid-clavicular line; it is rarely dislocated downward, and when so, not 
below the sixth intercostal space. Percussion reveals great increase in 
the deep cardiac dulness transversely, to the left slightly, and to the 
right considerably —2 to 5 cm. (f to 2 inches) beyond the right border of 
the sternum. The area is irregularly ovoid — transversely ovoid. On 
auscultation the heart sounds may be normal; the first sound usually is 
slightly dull and prolonged, and the second sound is accentuated or 
reduplicated in the pulmonary area. The pulse is usually regular, and 
increased in volume and tension. 

Hypertrophy of the auricles does not occur in the absence of asso- 
ciated disease of the ventricles or of valvular disease, and is scarcely 
to be diagnosticated in the absence of such associated disease. Hyper- 
trophy of the left auricle commonly causes enlargement anteropos- 
teriorly, since that the chamber of the heart, as a rule, does not come 
in contact with the chest wall; upon occasion, however, there may be 
some increased dulness in the third or the second left intercostal space, 



ANEURYSM OF THE HEART 443 

together with a visible and palpable presystolic (auricular systolic) pulsa- 
tion. Hypertrophy of the right auricle gives rise to dulness to the right 
of the sternum and a visible and palpable presystolic (auricular systolic) 
pulsation in the third and fourth right intercostal spaces, occasionally also 
in the third left intercostal space. 

With the onset of dilatation the apex beat grows weaker, more diffuse, 
and irregular; often, although a diffuse wave may be seen, none can be 
felt (or scarcely felt); the dulness is increased, especially to the right, 
the heart sounds lose their muscular element and become sharp, higher- 
pitched, valvular, and later quite feeble and indistinct. Murmurs 
of relative mitral and tricuspid insufficiency frequently develop; gallop 
rhythm may supervene; autochthonous pulsations appear in the jugular 
veins and the liver; the pulse becomes small, quick, and irregular; and 
other evidences of failing cardiac compensation develop. At times death 
occurs suddenly, and without premonition. 

Prognosis. — The prognosis depends upon the etiological factors and 
the associated conditions. Hypertrophy itself is a conservative process; 
so long as it remains efficient the outlook is good. From the nature of the 
process, however, the final prognosis is bad, since ultimately the nutrition 
does not keep pace with the enlargement of the heart, and degenerative 
processes and finally dilatation ensue. The prognosis in dilatation 
depends upon its cause and degree. 

Treatment. — The treatment of hypertrophy and dilatation is so 
intimately bound up with the causal factors that it can scarcely be dis- 
cussed apart from them. In general, an overactive hypertrophied 
heart is much benefited by rest, the avoidance of tobacco, coffee, tea, 
alcohol, etc., and the use of sedatives, such as the bromides, valerian, 
aconite, etc. The treatment of dilatation is that of decompensation 
in valvular disease. 



ANEURYSM OF THE HEART. 

Aneurysm may involve the myocardium or the valves. Valvular 
aneurysm may result from acute valvular endocarditis, which leads to 
softening and weakness of a leaflet, and permits of its distention in re- 
sponse to the influence of the blood pressure. This is most common at 
the aortic orifice, where the aneurysm usually forms an ovoid or spheroid 
projection into the left ventricle; rarely a similar condition occurs at the 
mitral valve. Rupture may occur and give rise to valvular insufficiency. 
Otherwise the condition cannot be recognized during life. 

Myocardial aneurysm may follow an area of localized weakening; 
this is usually due to fibroid myocarditis, a scar of a healed infarct, 
a gumma, mural endocarditis, etc. The common seat is the left ventricle 
near the apex. The aneurysm is usually saccular, rarely a rather diffuse 
dilatation. There are no characteristic symptoms. Occasionally 
there may be a localized pulsating prominence near the region of the 



444 DISEASES OF THE MYOCARDIUM 

apex beat, and an irregular area of dulness. The condition may be 
revealed by a Rontgen-ray examination. The prognosis is bad, rupture 
ensuing eventually. Treatment is unavailing. 



RUPTURE OF THE HEART. 

Rupture of the heart is a rare event that may occur in cases of degene- 
rated or softened myocardium. This occurs especially in aneurysm of the 
heart, in the fibroid heart, in the fatty heart, in softening (myomalacia 
cordis) due to obstruction (embolism or thrombosis) of the coronary 
artery, in suppurative myocarditis, gummas, ulceration endocarditis, etc. 
It occurs most commonly in men over sixty years of age, and is usually 
due to some exertion. The rupture may occur anywhere, but is most 
common in the wall of the left ventricle near the septum. Occasionally, 
also a valve leaflet may be ruptured and lead to valvular insufficiency; 
usually it results from severe exertion or traumatism to the chest, or from 
ulcerative endocarditis. The symptoms of rupture of the heart are rarely 
unequivocal. Usually there is sudden death without premonitory symp- 
toms. Occasionally there is sudden, perhaps agonizing, pain in the pre- 
cordium, a sensation as of something giving way in the chest, dyspnoea, 
anxiety, collapse, and death from the pressure of the ensuing hemoperi- 
cardium upon the heart; death may be delayed for twelve hours or 
more, rarely, even for days. The diagnosis is rarely made; it is sug- 
gested by the aforementioned symptoms and the physical signs of fluid 
in the pericardium. The prognosis is hopeless and treatment ineffectual. 



TUMORS AND PARASITES OF THE HEART. 

Tumors of the heart are rare; but lipoma, fibroma, myoma, sarcoma, 
and carcinoma have been observed. Sarcoma and carcinoma are 
usually secondary, and may be single or multiple. There are no sig- 
nificant symptoms; decompensation may ensue ultimately. 

Parasites of the heart also are rare. The most common is Echino- 
coccus granulosa. Cysticercus cellulosa?, Trichinella spiralis, Strepto- 
thrix actinomyces, etc., have also been observed. 



DISEASE OF THE CORONARY ARTERIES. 

Disease of the coronary arteries can scarcely be separated from 
disorders to which it gives rise or with which it is associated. The integ- 
rity of the myocardium, of course, depends upon an efficient coronary 
circulation — which may become disordered in toto or locally, slowly 
or suddenly. The chief consequences are: (1) Infarction and softening. 
This is due to occlusion of a larger or smaller twig (end artery), and is 






ACUTE ENDOCARDITIS 445 

most common in the area of distribution of the anterior coronary artery. 
The absence of such infarction in some cases of arterial occlusion is 
attributable to abnormal anastomoses or to an efficient circulation 
through the vessels of Thebesius. The softened infarcted area is gradu- 
ally replaced by scar tissue, which later may be the seat of an aneurysm 
or of rupture of the heart. (2) The fibroid heart (which see). (3) An- 
gina pectoris (which see). (4) Sudden death. A not uncommon cause 
of sudden death is occlusion of one coronary artery or of one of its main 
branches. The occlusion is usually due to thrombosis of a vessel 
somewhat sclerosed and more or less narrowed; the circulation has 
been perhaps for some time precarious, but, the final interruption of the 
circulation being rather sudden, death may ensue immediately. 



DISEASES OF THE ENDOCAKDIUM. 



ACUTE ENDOCARDITIS. 

Etiology. — Acute endocarditis is rarely a primary disorder; usually it 
is secondary to infectious processes elsewhere in the body. It occurs 
most frequently in association with rheumatic fever, the likelihood of 
its development increasing with recurrence of attacks of rheumatism; 
75 per cent, or more of endocarditic subjects are or have been rheumatic, 
and others give a history of such related disorders as tonsillitis (the portal 
of entry of the infectious agent), chorea, neuromuscular (growing) 
pains (especially significant in children), erythema nodosum, etc. 
Acute endocarditis occurs also in association with scarlatina, pneumonia, 
pyococcic, gonococcic, and typhoid infections, dysentery, influenza, 
and occasionally also with diphtheria, tuberculosis, measles, etc. The 
local lesions in the heart may be provoked by the primary infective agent, 
but frequently they are set up by secondary pyococcic invaders. The 
disorder is most common in adolescents and young adults, corresponding 
with the period of greatest prevalence of the aforementioned infections. 
It is predisposed to by diabetes, chronic nephritis, gout, syphilis, carci- 
noma, and chronic anemic and debilitating disorders in general, and in 
consequence it is not uncommonly a terminal event in older subjects. 
It is often engrafted on an old or chronic endocarditis. 

Pathology. — Different types or forms of the disease may be distin- 
guished — rheumatic, staphylococcic, streptococcic, pneumococcic, gono- 
coccic, typhoid, influenzal, etc.; simple (or benign) and ulcerative (or 
malignant); verrucose and ulcerative; and valvular and mural. Except 
etiologically, no sharp, line of demarcation can be drawn between these 
types. 

The lesions are most common in the left side of the heart, the relative 
frequency being as follows: The mitral valve in 50 per cent, or more of 



446 DISEASES OF THE ENDOCARDIUM 

the cases when affected alone, in 80 per cent, when associated with lesions 
elsewhere; the aortic valve in 15 per cent, when affected alone, in 40 per 
cent, when associated with lesions elsewhere; the tricuspid valve; the 
pulmonary valve; the wall of the left auricle and ventricle; and the wall 
of the right auricle and ventricle. Endocarditis developing during 
intra-uterine life is more common in the right side of the heart, which 
fact is attributed to the greater strain and stress to which the right and 
the left side of the heart respectively is subjected in intra-uterine and 
extra-uterine life; there are, however, other more or less ill-understood 
factors, such as anomalies of development, etc. 

In the simplest form, the lesions consist of small, grayish, translucent 
vegetations or excrescences attached to the line of closure of the valves, 
that is, to the surface opposed to the blood current, the auricular surface 
of the mitral valve, and the ventricular surface of the aortic valve. Often 
the vegetations are extremely small, 1 to 2 mm. in diameter, bead-like; 
they may be larger, and have a fissured or wart-like surface; sometimes 
they are attached by a pedicle, that is, polypoid. They are most commonly 
situated along the line of closure of the valves, which appears to be re- 
lated to the fact that the regions most exposed to strain and traumatism 
are most likely to be less resistant, and that the infection is probably 
effected through the medium of the blood circulating through the 
cavities of the heart, rather than that circulating in the coronary vessels, 
although this is still a debated point. The vegetations developing on the 
valves may spread to the chordae tendinese, the wall of the cavities, etc. 
They consist for the most part, of fibrin, leukocytes, and blood platelets 
(coagulable elements of the blood), superimposed upon an area of 
desquamating and proliferating endothelial cells. Occasionally there 
is a surrounding area of reactive congestion, but often this is entirely 
absent. The causative microorganisms may be found in the vegetations, 
but they are not infrequently absent when sought — which suggests that, 
having initiated the lesions, the microorganisms may die out, or, as is 
likely, that toxins suffice to set up the lesions. Insufficiency of the valve 
is a common concomitant, being the result of malposition of the leaflets 
dependent upon the vegetations or upon a consecutive deformity of the 
leaflets; but when the vegetations are small the insufficiency is often due 
less to the vegetations per se than to myocardial disorder and inter- 
ference with the normal action of the valve leaflets and papillary muscles. 

The subsequent course of events varies: (1) In the course of time 
the proliferating endothelial cells and fibroblasts may invade the vegeta- 
tion, and by a process akin to organization gradually lead to its replace- 
ment, so that ultimately the lesion is represented by a scar. In rare cases, 
in which the lesions have been minor in grade, restitution to the normal 
may perhaps ensue; but this is doubtful, and very unlikely in a given case. 
The scar usually contracts and leads to thickening, induration, and 
distortion of the valve leaflets — chronic valvular disease. (2) The lesions 
may progress to what is often spoken of as ulcerative or malignant 
endocarditis. This, merely an aggravation of the more benign lesion, 



ACUTE ENDOCARDITIS 447 

usually begins on the valves, but it is likely to spread to the chordae ten- 
dinese and the mural endocardium, and while it is most frequent in the 
left side of the heart, it is not uncommon also in the right side. It is char- 
acterized not only by the most exuberant vegetations, but also by more 
or less extensive necrosis and ulceration of the underlying tissues; so 
that to the previously existing valvular insufficiency, stenosis of the orifice 
(from blockage by vegetations) is not infrequently added. The ulcera- 
tion may be superficial, involving perhaps only the endocardium; but 
usually it is more extensive, and not uncommonly leads to aneurysmal 
dilatation and perforation of a valve leaflet, destruction of the chordae 
tendinese or papillary muscles, perhaps considerable necrosis, suppura- 
tion, even perforation of the cardiac septa or walls. The lesions may 
also spread to the aorta and the pulmonary vessels. The vegetations are 
likely to become disintegrated, and being detached in part or in whole 
and swept into the circulation, cause embolism and infarction in differ- 
ent organs, especially the spleen, kidneys, brain, intestine, etc. (or in 
the lung in involvement of the right side of the heart). Multiple abscesses 
(so-called arterial pyemia) ensue, if the emboli are infected. The 
lesions in the heart thus are often relatively insignificant, being over- 
shadowed by those of the primary disorder and the metastatic phe- 
nomena. Often the cardiac lesions are widespread, involving the 
endocardium, the myocardium, and the pericardium, so that the term 
pancarditis is most appropriate. 

Symptoms. — The milder grades of acute endocarditis frequently run 
their course entirely unsuspected; of themselves they occasion no note- 
worthy or unequivocal symptoms, and frequently are disclosed only by 
the necropsy. Since the disease is especially common in rheumatic 
fever, the likelihood of its occurrence should be borne in mind; its 
development should be suspected in the event of precordial distress or 
oppression, palpitation, dyspnoea on slight exertion, rapid and irregular 
cardiac action, and persistence or sudden increase of fever without 
adequate articular or other signs to explain it. The more marked 
grades of the disorder exhibit gradual progression in symptomatology 
to that of frank septicopyemia — irregular chills, fever (remittent or high 
and continuous), sweats (often profuse), rapid loss of flesh and strength, 
progressive anemia, polynuclear leukocytosis, enlargement of the spleen, 
diarrhoea, pyococcic or other bacteremia, etc. These phenomena are 
not essentially different, whether they occur in septicopyemia attended 
or unattended with endocarditis; but they are especially significant if 
there be no adequate cause to explain them, or if they occur in a subject 
of old valvular disease. 

In most cases the diagnosis depends upon the occurrence of embolic 
phenomena and the results of a physical examination of the heart. Of 
embolic phenomena the most important and suggestive occur in the 
skin — petechias; in the kidneys — renal pain, albumin, blood, and tube 
casts in the urine; in the spleen — splenic pain, palpable and audible 
frictions; in the lungs — pain, hemoptysis, perhaps localized dulness, 



448 DISEASES OF THE ENDOCARDIUM 

bronchial breathing, and fine rales; in the cerebrum — hemiplegia 
monoplegia, aphasia, blindness, convulsions; in the eye — retinal hemor 
rhages and optic neuritis, as well as petechial hemorrhages in the palpe 
bral conjunctiva; in the long bones — local pain and tenderness; u 
the joints — local pain, swelling and tenderness; painful ephemera 
erythematous nodules in the fingers, toes, hands, and feet; and in the 
extremities — gangrene from vascular obstruction. The joint symptoms 
are often fugitive and much resemble the articular manifestations of 
rheumatism; they are doubtless toxic in nature, as are also some of 
the skin manifestations, such as certain roseolas, erythemas, urticarias, 
etc. 

The extreme variability in the symptomatology has led to a classifica- 
tion of the disorder into several types: (1) The cardiac type, in which 
cardiac distress and obvious valvular lesion with attendant failure of 
cardiac compensation constitute the noteworthy features; (2) the septic, 
or pyemic type, which cannot be distinguished from septicopyemia, of 
which in reality it is a manifestation; (3) the typhoid type, resembling 
typhoid fever in the toxemia, asthenia, and prostration; and (4) the cere- 
bral type, resembling meningitis. These terms, however, are largely 
misnomers, since the disease necessarily is always cardiac and toxemic 
or septicopyemic, and the irregularity and multiplicity of the lesions and 
symptoms do not really permit of such classification. 

The physical signs are extremely uncertain. In some cases there may 
be no discernible deviation from the normal, especially in some of the 
streptococcic, gonococcic, and pneumococcic forms. The cardiac action 
is often persistently excited (without obvious adequate cause), and 
sometimes peculiarly unstable, attacks of tachycardia (120 to 150 heart 
beats per minute) often developing suddenly and ceasing quite as sud- 
denly (without apparent cause); this is of some diagnostic importance. 
In some cases the first sound at the apex becomes impure or muffled, and 
finally replaced by a murmur, and other signs of mitral insufficiency 
develop; in other rarer cases the signs of aortic insufficiency or other 
valvular defect ensue. Extreme variability in the character of the 
murmur from day to day (perhaps related to changes in the vegeta- 
tions, or due to incoordinated action of the papillary muscles) is quite 
significant, but is not always present. 

The clinical course of the disease is quite variable, but permits of 
grouping of the cases : (1) Mild cases, which are common in rheumatic 
fever, and occur also in typhoid fever and other infections and in de- 
bilitated conditions, perhaps as a terminal infection. The clinical phe- 
nomena are slight or altogether absent, but if the patient survives, the 
lesions usually lead to chronic valvular disease. (2) Severe cases, which 
are especially common in pyococcic infections (puerperal infection, wound 
infection, pneumonia, gonorrhoea, scarlatina, etc.), although they may 
occur also in milder infections, rheumatic fever, etc. The clinical phe- 
nomena may be more or less obtrusive, and the lesions may subside leav- 
ing a valve or valves more or less damaged; or a fatal result may ensue 









ACUTE ENDOCARDITIS 449 

within several weeks; or a chronic septic process may be set up and 
continue for months. (3) Recurring or relapsing cases, which may be 
interpreted as relighting of an obsolete infection or reinfection of a 
damaged valve — a form of chronic endocarditis. 

Diagnosis. — The diagnosis of the simple or mild cases is difficult, and 
is often a matter merely of conjecture. Increase of the cardiac dulness, 
an apical systolic murmur, and an accentuated pulmonic second sound 
are not uncommonly due to toxic degeneration of the myocardium 
provoked by divers infections (rheumatic fever, etc.). The gradual 
development of the murmur is suggestive of endocarditis; but since anemia 
and degeneration of the myocardium usually supervene at about the 
time endocarditis may develop, the diagnosis cannot always be made, 
and often must await the passage of time; persistence of the physical 
signs after convalescence from the infection, of course, is conclusive 
evidence of a valvular defect. The development of a diastolic murmur 
during the infection is of itself almost conclusive of aortic endocarditis. 
The diagnosis of the more severe cases may be based upon the symptoms 
of septicopyemia, embolic phenomena, and the physical signs referable 
to the heart already mentioned. In obscure cases blood cultures may 
afford material diagnostic assistance. 

Typhoid fever may be excluded by the absence of the prodromes, 
especially the persistent headache and nose-bleed, roseola, tympanites, 
delirium, dry tongue, Gruber-Widal reaction, and typhoid bacilli from 
the feces, urine, roseola, and blood, and by the presence of a source of 
infection, irregular and repeated rigors, intermittent fever, profuse perspi- 
ration, rapid and unstable pulse, undue dyspnoea, the early occurrence 
of marked prostration, the rapid development of anemia, leukocytosis, 
embolism, and the detecting of the infecting microorganism in the blood. 
The spleen is said to become less enlarged, although more tender, in 
endocarditis (and sepsis) than in typhoid fever. It is well also to bear 
in mind that the typhoid bacillus may set up the endocarditis, either 
primarily or by infecting an old lesion. In acute tuberculosis, as con- 
trasted with acute endocarditis, variations in the temperature and pulse 
rate, and excessive perspirations occur with more regularity, wasting 
is more rapid, a local focus of tuberculous disease may be detected in 
some part of the body — in the lungs (tubercle bacilli in the expectora- 
tion), in the pleura, in the abdomen, in the brain (tubercle bacilli in the 
cerebrospinal fluid obtained by lumbar puncture), etc. ; physical examina- 
tion of the heart reveals no signs of valvular disease (except in the rare 
cases in which there is an associated valvular lesion); and embolism 
does not occur. The detecting of choroidal tubercles in the one case, 
and of retinal hemorrhages in the other, is of the greatest diagnostic 
value. Malaria may be excluded by the irregularity of the attacks 
of chills, fever, and sweats, polynuclear leukocytosis, absence of malarial 
plasmodia from the blood, and the administration of quinine. 

Prognosis. — The prognosis varies with the severity of the lesions — 
which has already been referred to. The seriousness of the lesions, 
29 



450 DISEASES OF THE ENDOCARDIUM 

however, sometimes cannot be judged from the clinical manifestations, 
so that for a time at least the prognosis as regards life may be doubtful ; 
that as regards the heart is always bad, since chronic valvular disease 
almost certainly results. Rarely even severe so-called malignant endo- 
carditis may eventuate in recovery, with more or less permanent damage 
to the heart. Usually, however, it ends in death, or the acute symptoms, 
fever, etc., subside within two or three months. 

Treatment. — The treatment resolves itself largely into that of the 
primary infection — whether rheumatic or non-rheumatic. It is perhaps 
possible in some cases of rheumatism, to prevent the development of 
endocarditis — by prompt and efficient treatment of the rheumatism. 
The patient should be absolutely at rest in bed, and should be brought 
promptly under the influence of the salicyl preparations — large doses 
to the point of mild intoxication. This not only relieves the rheumatic 
manifestations, but, counteracting the poison it should tend to prevent 
the occurrence of endocarditis; there is some evidence that it does. 
Some observers believe that the addition of the alkalies (in twice the dose 
of the salicyl preparation) is of much value. Caton insists on the 
importance also of small repeated blisters to the precordium, and he as 
well as others extol the advantage of prolonged rest in bed — six weeks 
to three months. 

The treatment of developed endocarditis also is largely that of the 
primary disorder — in rheumatic cases that just mentioned; in other 
cases, that of the initiating pyococic, gonococcic, pneumococcic infection, 
etc. Should it be possible to cultivate the provoking microorganism 
from the blood, a vaccine may be prepared and used with hope of good 
result. The serums used heretofore have not been especially successful. 
Colloidal silver also is scarcely to be recommended. Indeed, in severe 
cases, it is doubtful if any measures, aside from general supportive, 
can achieve much good. In the event of palpitation or cardiac distress 
an ice-bag should be applied to the precordium, or aconite may be used 
in small doses. 

CHRONIC ENDOCARDITIS. 

Etiology. — Acute endocarditis, if it does not lead to death, usually 
subsides within two or three months, and leaves the cardiac valves per- 
manently damaged (chronic valvular disease), although rarely the 
lesions may be limited to the mural endocardium. In a few cases, how- 
ever, the endocarditic phenomena are protracted — for many months; 
and in many cases, having become more or less quiescent, they 
are relighted (recurring or relapsing endocarditis). The etiological 
factors in these chronic cases are the bacterial agents that set up acute 
endocarditis; but the later attacks in the recurring cases are not always 
provoked by the bacterial cause of the primary attack; the damaged 
valves are especially vulnerable to the attack of any pathogenic bacterium. 



CHRONIC ENDOCARDITIS 451 

Pathology. — The lesions vary much in different cases. In most cases 
(relapsing form) they consist of the various lesions more particularly 
described under valvular disease, to which the lesions characteristic 
of acute endocarditis are added; in some cases to the deformity of the 
valve, more or less exuberant, sometimes rather firm, vegetations are 
added; in other cases there are more or less superficial or deep ulcerations. 

Symptoms. — The symptoms in general are like those of acute endo- 
carditis, but protracted or recurrent. In one series of cases (chronic 
recurrent or relapsing endocarditis), aside from the symptoms due to the 
associated valvular disease, there are recurring attacks of chills, fever, 
and sweats, and leukocytosis (mild septicopyemia), with intervening 
periods of good health. During the attack the cardiac symptoms may 
be in abeyance, or those previously present may become aggravated, 
and the embolic phenomena of acute endocarditis may supervene. In 
another series of cases the symptoms are continuous from the beginning; 
they do not differ essentially from those of acute endocarditis, although 
perhaps they are less severe; but rarely chills, fever, sweats, and leuko- 
cytosis may last for months. In certain rare and protracted cases per- 
sistent fever (100° to 102°) is the characteristic and dominant mani- 
festation; chills and sweats are much less common than in the acuter 
cases, but they may occur from time to time, and are then usually 
associated with an added increment of fever. Occasionally, after the 
lapse of months, the lesions may subside and the patient become apy- 
retic, but recurrence of the symptoms is likely. Rarely there is a slight 
cough and the patient may emaciate (suggesting tuberculosis). There 
are usually the physical signs of mitral or aortic valve disease, although 
occasionally for long periods or throughout the disease there may be 
no murmur whatever. Embolic phenomena occur, but they are less 
common than in the acuter forms of the disease. 

Diagnosis. — The basis of a diagnosis is the same as that of acute 
endocarditis; but special importance attaches to the knowledge of an 
old valvular disorder, increase in the size of the heart, changes in the 
character of the cardiac murmurs, the development of new murmurs, 
embolic phenomena, recurring attacks of fever, etc. In cases that 
present little else than persistent fever it may be quite impossible for 
some time to eliminate typhoid fever or tuberculosis. A blood culture 
may reveal the nature of the infection. Malaria should be readily ex- 
cluded. 

Prognosis. — The prognosis is bad. Rarely cases in which the symp- 
toms continue unabated from the beginning may last a year or more. 
The relapsing cases may continue for several years, the duration being 
determined by the periods of apyrexia, the permanent damage done 
to the cardiac valves, and the ensuing changes in the myocardium. 

Treatment. — The treatment is that of acute endocarditis plus that of 
the associated valvular disorder. 



452 DISEASES OF THE ENDOCARDIUM 



CHRONIC VALVULAR DISEASE OF THE HEART. 

Etiology. — Two types of chronic valvular disease of the heart may be 
distinguished: (1) The chronic inflammatory, and (2) the arterio- 
sclerotic or atheromatous; but a sharp line of distinction cannot always 
be drawn between them, and the final lesions in both are much alike. The 
first or chronic inflammatory iype most frequently involves the mitral 
valve, is most common in young subjects and in women, and usually 
results from acute endocarditis; the causes of the one, therefore, are the 
causes of the other, the chronic lesions representing the results of healing 
of the acute process. In a minority of the cases, the lesions may be 
chronic from the beginning, initiated perhaps by the toxins of attenuated 
microorganisms or by certain ill-understood autotoxins. The second, 
arteriosclerotic or atheromatous type, most frequently involves the 
aortic valve, is most common in male adults, and occurs with increasing 
frequency in both sexes as the subjects advance in years. The especially 
important etiological factors are alcoholism, syphilis, and excessive and 
long-continued muscular strain, but it is due also to gout, plumbism, 
chronic nephritis, diabetes, and the divers other factors related causally 
to arteriosclerosis and high arterial tension. In some cases, especially 
of mitral valve disease, no etiological factor can be determined with 
certainty. A few cases, especially of aortic valve disease, are apparently 
traumatic in origin, developing in consequence of sudden undue muscular 
strain, severe contusions or compression of the chest, etc., which lead 
directly to rupture of a valvular leaflet. Heredity seems to play a role 
in some cases. Lesions of the right heart are usually congenital. Acute 
lesions are not infrequently superadded to the chronic: this may be a 
frank acute, more or less severe (or malignant) endocarditis, due usually 
to the pyococci ; or it may be the relighting of a more or less quiescent or 
obsolete infection (recurring or relapsing endocarditis). 

Pathology. — Among 1058 cases collected by Parrot, the mitral valve 
was involved in 621 (58.7 per cent.), the aortic in 380 (36 per cent.), 
the tricuspid in 46 (4.3 per cent.), and the pulmonary in 11 (1 per cent.); 
the left side of the heart in 1001 (94.7 per cent.), the right side of the 
heart in 57 (5.3 per cent.). In minor or slight cases the lesions consist 
of opacity, or of slight, perhaps nodular, thickening and induration near 
the free margin of the valve leaflets, just within the margin in mitral 
and tricuspid disease, and about the corpora aurantii in aortic disease; 
these may be interpreted as the results of so-called organization of the 
acute vegetations, or as the analogue of the early changes of arteriosclero- 
sis (which may be associated). The body of the valve leaflets may reveal 
grayish-white opacities or yellowish areas of fatty degeneration. The 
newly formed fibrous tissue, of which the opacities and thickenings are 
made up, gradually undergoes contraction and leads to varying degrees 
of curling or puckering of the edge of the leaflets, or of stiffness, indura- 
tion, shortening, and deformity of the leaflets as a whole. On account of 



CHRONIC VALVULAR DISEASE OF THE HEART 453 

the consequent lack of resiliency the leaflets do not approximate properly, 
or on account of shortening, they do not approximate at all, and the 
condition known as insufficiency of the valve ensues. In the case of 
the auriculoventricular (mitral) valve this is often due to or augmented 
by involvement in the sclerotic and contracting process of the chordse 
tendinese and tips of the papillary muscles. In the course of time the 
adjacent edges of the leaflets often become adherent, in consequence of 
which their movement is still further restricted, and not receding as they 
should normally, they oppose a barrier to the onward movement of 
the blood — so-called stenosis or obstruction. Calcium salts frequently 
become deposited in the sclerotic and necrotic tissues, and add to the 
already existing rigidity of the leaflets. In advanced cases the normal 
tissues of the valves may be entirely replaced by a firm, fibrous, resistant 
calcareous mass capable of scarcely any movement, so that the valves 
are insufficient and the orifice stenosed. The lesions sometimes spread 
from the valves to the mural endocardium; rarely the mural endocardium 
alone is involved, a larger or smaller indurated, cicatricial, and perhaps 
calcareous patch being present. Superadded to the chronic, acute 
lesions are sometimes found. Hypertrophy and dilatation of the heart, 
varying grades of myocarditis, and coronary sclerosis are almost constant 
concomitants. 

Pathological Physiology. — The heart and bloodvessels are so adjusted 
to the actual and potential work required of them, that in health and 
under the stress of unusual temporary functional demands, the required 
work is performed without discomfort to the patient. Sudden increased 
demands, such, for instance, as are developed during strenuous exercise, 
lifting unusually heavy weights, etc., are met with increased rapidity of 
the heart action; often slight dilatation of the heart ensues, but being- 
well within the limits of the so-called reserve power of the heart, no 
serious consequences ensue; with the accomplishment of the work the 
dilatation subsides and the heart's action returns to the normal. Should 
the demands be more continuous, although perhaps less onerous, the 
heart responds, as does the musculature throughout the body, by hyper- 
trophy, and the persisting dilatation that otherwise would ensue is 
counteracted , the equilibrium of the circulation is maintained : the lesion 
is said to be compensated. In valvular disease, in consequence either 
of orificial obstruction to the onward flow of the blood or of insufficiency 
of valves permitting regurgitation of the blood, the primary dilatation 
and consecutive hypertrophy involve first that chamber of the heart im- 
mediately back of the valve or orifice affected — the auricle in mitral and 
tricuspid valve disease, and the ventricle in aortic or pulmonary valve 
disease. Hypertrophy may not develop when the myocardium has be- 
come enfeebled in consequence of long-continued fever, general debilitat- 
ing conditions, such as marked anemia, diabetes, carcinoma, amyloidosis, 
fibroid degeneration, etc. The hypertrophy when it does occur is 
sufficient to maintain the equilibrium of the circulation for a longer or 
shorter period, but it is not permanently efficient; to the hypertrophy 



454 DISEASES OF THE ENDOCARDIUM 

dilatation is gradually added, and as the dilatation, in consequence of 
insufficient nourishment and consecutive degeneration of the hyper- 
trophied myocardium, assumes the ascendency, the period of compensa- 
tion is supplanted by a period of unstable compensation, and finally by a 
period of failure or lack of compensation (decompensation). During 
the period of compensation the valvular disorder is disclosed only by its 
physical signs or by a lessened ability on the part of the heart to respond 
to unusual demands without discomfort to the subject (dyspnoea, cyan- 
osis, palpitation of the heart, etc.) ; this the consequence of lessened reserve 
power. Gradually, as the myocardium becomes enfeebled, it becomes 
less able to withstand the vicissitudes of ordinary life, and it dilates. 
The ensuing loss of compensation may develop suddenly and rapidly 
lead to death; usually it is of gradual onset and progressive; it may be 
temporary or permanent. For a time the heart is manifestly adequate 
to meet the demands of quiet life, but more or less distress (dyspnoea, 
cough, cyanosis, palpitation of the heart, precordial pain, vertigo, faint- 
ness, slight and transient oedema about the ankles, etc.) ensues upon 
exertion, excitement, a full meal, etc.; but the symptoms subside upon the 
restoration of quiet: the compensation is unstable. Sooner or later the 
heart becomes unable to maintain the equilibrium of the circulation 
even when the body is at rest; the aforementioned symptoms become 
more or less permanent: the compensation is lost. This condition may 
eventuate in death; but in many cases the symptoms gradually subside 
temporarily, and are followed by recurring relapses and partial or more 
or less complete recoveries. 

The first evidences of this failure of compensation are manifest in that 
part of the cardiovascular system immediately back of the chamber 
of the heart primarily involved: in valvular disease of the left side of the 
heart, therefore, in the lungs; but in most cases the lungs have been for 
some time engorged, so that speedily the congestive and other disturb- 
ances become manifest in the general venous system throughout the body. 
At the same time, failure of compensation becomes apparent in front of 
the lesion in a lessened and irregular blood supply. The evidences 
of lack of compensation, then, are disclosed not so much by the physical 
signs referable to the heart, although these are important, as by the 
evidences of general venous and capillary stasis and a small, weak, fre- 
quent, and irregular pulse. 

The ordinary mechanism of valvular insufficiency and stenosis is that 
already described. Under other circumstances, however, the valvular 
orifices dilate, and normal leaflets become, therefore, incompetent to 
close the enlarged orifice — a condition spoken of as relative insufficiency, 
and very common at the mitral and tricuspid orifices . It doubtless occurs, 
but is very rare, at the aortic and pulmonary orifices. Relative ob- 
struction (or stenosis) is occasionally produced by exuberant vegetations, 
ball-valve thrombus, aneurysmal dilatation of a leaflet, etc. ; and a condi- 
tion sometimes spoken of as relative stenosis ensues when the cavities 






CHRONIC VALVULAR DISEASE OF THE HEART 455 

become much dilated while the orificial ring remains normal or is rela- 
tively only slightly enlarged. 

Mitral Insufficiency. — Mitral insufficiency is the commonest lesion, 
occurring alone in about 30 per cent, or more of the cases; mitral stenosis 
occurs in about 16 per cent., and both lesions in about 12 per cent. 

Etiology. — Mitral insufficiency may result from one of three factors: 
(1) Acute or chronic endocarditis. This is the common cause of the 
disorder in young persons; usually it is a sequel of rheumatism, "growing 
pains," chorea, scarlatina, and other infections. The mitral leaflets 
may be thickened, indurated, curled up at the edge, or everted, and con- 
tracted or puckered (the contraction and thickening may also involve 
the chorda? tendinese), so that the leaflets cannot be approximated; or 
more or less of one or both leaflets and the adjacent chordae tendinese 
may be eroded or destroyed; rarely a leaflet may be perforated. In 
some cases the adjacent margins of the leaflets become adherent, and 
as the newly formed connective tissue contracts, the leaflets are drawn 
together, so that to the insufficiency obstruction is added. Acute lesions 
are not uncommon (recurring or relapsing endocarditis). (2) Slowly 
progressing sclerosis, analogous to arteriosclerosis. This is a less common 
form; it is due to the ordinary causes of arteriosclerosis, and is found 
in adults and elderly persons. The leaflets and the chorda? tendinese 
are usually thickened and contracted, and the seat of more or less well- 
marked atheroma with calcification. Associated obstruction is not 
uncommon (12 per cent, of the cases). Minor grades of atheroma 
of the mitral valve are common in persons upward of sixty years of age, 
but usually do not lead to valvular defects. (3) Dilatation of the mitral 
ring. This, so-called relative or muscular insufficiency, is perhaps the 
commonest form. It is found in a wide variety of disorders in which 
the myocardium becomes reduced in tone and permits of such dila- 
tation of the mitral ring, and usually also of the left ventricle, that the 
normal mitral leaflets are unable to close the orifice: anemic conditions, 
infectious fevers, hypertrophy and dilatation of the heart, aortic valve 
disease, arteriosclerosis, chronic nephritis, chronic myocarditis, nervous 
disorders, such as exophthalmic goitre, etc. 

Pathological Physiology. — In consequence of incompetency of the 
mitral valve, a portion of the ventricular blood, varying in amount with 
the degree of incompetency, is returned to the left auricle during the 
ventricular systole, that is, at a time when the auricle in diastole is 
receiving blood normally from the lungs. The immediate result of this 
is an abnormal rise of the intra-auricular pressure toward the end of 
auricular diastole and consequent dilatation of the left auricle. The 
tension and stretching to which the auricular musculature is thus sub- 
jected stimulate it to vigorous contractions, in an effort to expel the 
augmented amount of blood, and the constant recurrence of the stimu- 
lus ultimately induces more or less hypertrophy. The regurgitating 
stream impedes the flow of blood from the pulmonary veins into the left 
auricle and leads immediately to stasis in the pulmonary circulation — 



456 DISEASES OF THE ENDOCARDIUM 

since the pulmonary veins are unprovided with valves, and the supposed 
constriction of the musculature at the insertion of the pulmonary veins 
into the auricle cannot long remain active or oppose an effective barrier 
to back pressure into the lungs. The increased pulmonary pressure acts 
as an obstruction to the movement of blood from the right heart and 
stimulates the right ventricle to more vigorous contractions and soon 
leads to hypertrophy — which is the effective factor in maintaining com- 
pensation. The increased volume of blood injected into the left ventricle 
with each auricular contraction leads to a corresponding dilatation of 
the left ventricle; this, in turn, is followed by more vigorous contractions 
in an effort to discharge the augmented volume of blood, so that ulti- 
mately some hypertrophy of the left ventricle ensues, but in uncom- 
plicated mitral insufficiency this is rarely marked. So long as the 
hypertrophy of the right ventricle remains efficient, the mitral lesion is 
compensated and the patient may not suffer any distress. Sooner or later, 
however, the musculature weakens and dilates, either in consequence 
of myocardial degeneration or of increase in the mitral lesion; and 
relative insufficiency of the tricuspid valve ensues. The back pressure 
then is communicated to the right auricle and the liver and the general 
venous system. In mitral insufficiency the lungs are always engorged, 
and ultimately the condition of cyanotic induration develops (congestion 
and dilatation of the bloodvessels, hemorrhages, pigmentation, and fibro- 
sis); the larger pulmonary vessels may exhibit atheromatous changes. 
When the back pressure finally involves the general venous circulation, 
passive congestion ensues, and in the course of time leads to oedema 
of the subcutaneous tissues, chronic catarrh of mucous surfaces, cyanotic 
induration of solid organs, transudates in the serous cavities, etc. 

Symptoms. — Well-compensated mitral insufficiency may be disclosed 
only by a physical examination of the heart; there may be no subjective 
symptoms whatever, although usually some little embarassment of respi- 
ration and hurried action of the heart ensue upon sudden or severe 
exertion, such as hill climbing, ascending stairs, or strenuous exercise. 
In the majority of cases, however, the patient, although not seriously 
embarassed during ordinary activities, is made aware of his cardiac 
deficiency upon any unusual exertion; others may lead a quiet life with 
comfort, but even minor activities induce cardiac distress — which ex- 
erts its chief effects on the pulmonary circulation, and becomes mani- 
fest in palpitation of the heart, precordial distress, dyspncea, and slight 
cyanosis of the cheeks, lips, ears, and finger tips. The congestion of the 
lungs disposes to attacks of bronchitis, which are readily induced by 
seasonal and climatic changes, and to attacks of hemoptysis (less fre- 
quent than in mitral stenosis). In long-standing cases that develop in 
youth, the finger tips tend to become clubbed. 

Sooner or later the heart begins to fail, more or less complete, temporary 
or permanent, loss of compensation ensues; the passive congestion of the 
lungs becomes more marked, and to this is added the evidences of general 
venous and capillary stasis. The patient complains of palpitation, and 






CHRONIC VALVULAR DISEASE OF THE HEART 457 

the heart action becomes rapid, irregular, and weak. More or less cyan- 
osis develops. Dyspnoea, cough, and perhaps expectoration are expres- 
sions of the increased pulmonary engorgement; the expectoration is 
usually mucous, sometimes watery or serous, occasionally streaked with 
blood; usually it contains pigmented alveolar epithelial cells (so-called 
heart disease cells). The congestion of the liver (enlarged and tender) may 
lead to slight jaundice or lend a subicteric hue to the conjunctivae and the 
skin. Dropsical effusions supervene, at first in the subcutaneous tissues 
in the dependent portions of the body. For a time they are transitory, 
developing during the day when the patient is up and about, and dis- 
appearing when he is in bed; but they soon become more or less perma- 
nent, although fluctuating; they may involve the general subcutaneous 
tissues (anasarca), and may occur also in the serous cavities of the body. 
The right pleura is most frequently involved — four or five times as fre- 
quently as the left, and when there is bilateral involvement, the collec- 
tion of fluid is usually greater in the right side. This was attributed by 
Steele and Stengel to pressure on the azygos veins by the dilated right 
auricle; more recently Fetterolf and Landis, stating their belief that the 
fluid comes, not from the parietal, but from the visceral pleura, attribute 
the pressure factor to compression and partial occlusion of the pulmonary 
veins by dilated portions of the heart — dilatation of the right auricle in 
right-sided transudations, and dilatation of the left auricular appendix 
and of the left ventricle, and perhaps also retrodisplacement of the 
ventricular septum, in left-sided transudations. The urine becomes 
reduced in amount and contains a trace of albumin and often erythro- 
cytes and tube casts. Insomnia, often distressing, and perhaps slight 
delirium at night may develop. Usually there are recurring attacks 
of such failure of compensation; under appropriate treatment the 
patient recovers and may again enjoy good health. Eventually, how- 
ever, compensation becomes permanently lost and the patient dies of 
gradually increasing cardiac weakness and dilatation; but sudden death 
may ensue. 

Physical Signs. — Depending upon the youth of the subject when the 
disorder developed and the degree of hypertrophy of the right ventricle, 
there is more or less bulging of the precordium; the cardiac impulse 
is forcible and widespread, often especially conspicuous toward the 
sternum or in the epigastrium; the apex beat (the palpable beat farthest 
outward and downward) is displaced outward transversely (usually 
not downward in uncomplicated mitral valve disease); it is of in- 
creased breadth and not infrequently somewhat heaving in character. 
A systolic thrill may be palpable at the apex, and sometimes the forcible 
closure of the pulmonary valve may be palpable in the pulmonary area 
as a diastolic shock. The deep (and the superficial) cardiac dulness 
is increased transversely — somewhat to the left, but mostly to the right, 
forming a transverse oval that may extend one to two inches or more to 
the right of the sternum. Sometimes there is an increase of the dulness 
upward and outward from the left edge of the sternum — attributable to 



458 DISEASES OF THE ENDOCARDIUM 

enlargement of the left auricle (but enlargement of the left auricle is 
usually predominantly fore and aft, and usually causes little if any in- 
crease in dulness upward). At the apex a systolic murmur is usually 
audible — soft and blowing in character and low pitched, but it may 
be harsh and high pitched or musical; it may partly or completely replace 
the first sound; it may be audible only in the early part of systole (when 
it often progressively diminishes in intensity), or it may continue through 
the entire systole; its point of maximum intensity is usually directly 
over the apex (transmitted through the contracted left ventricular 
musculature); it is often transmitted to the axilla and the angle of the 
scapula (which is not of much importance diagnostically); rarely it is 
heard best along or near the left edge of the sternum, or in the fourth 
or the third, sometimes the second, interspace (pulmonary area) — in 
consequence of the direction of the blood current and of the auricle 
being in close contact with the chest; rarely it is heard best in the back 
between the scapulae; it is often loudest when the patient is recumbent; 
sometimes it is heard only when he is recumbent. The pulmonic second 
sound is accentuated, sometimes reduplicated. The pulse during 
compensation is not characteristic; it is full and regular, although 
perhaps of low tension. Occasionally in extreme insufficiency with 
considerable ventricular hypertrophy a pulmonary pulsation, a diffuse 
systolic expansion of the lungs (analogous to the liver pulsation of 
tricuspid insufficiency), may be palpable. With failure of compensation, 
the pulse becomes small, frequent, and irregular; the physical signs 
of cardiac dilatation assume the ascendency; the systolic murmur 
changes in character, lessens in intensity or disappears entirely, or 
perhaps is audible only during the stronger systoles that characterize 
the arrhythmia; the pulmonary second sound loses its accentuation, 
and the signs of relative tricuspid insufficiency, general venous engorge- 
ment, and oedema develop. 

Diagnosis. — The characteristic diagnostic signs consist of enlarge- 
ment of the right ventricle, a systolic thrill and a systolic murmur at the 
apex, and an accentuated pulmonic second sound. Relative mitral 
insufficiency is to be differentiated from organic insufficiency, not by 
the physical signs, which may be alike in both, but by the antecedent 
conditions and associated phenomena, by the presence of an adequate 
causative factor to give rise to dilatation of the heart and a relative mitral 
insufficiency, and by the disappearance of the murmur with improve- 
ment in the condition of the heart (lessening of the area of dulness, and of 
dilatation, and increase of vigor). The systolic murmur of aortic stenosis 
is sometimes very loud at the apex, but it is loud also at the aortic area 
and is propagated into the carotid artery, and it is associated with the 
other distinctive signs of aortic stenosis. Difficulty is not infrequently 
experienced in differentiating so-called functional, inorganic, accidental, 
or hemic murmurs, as well as certain exocardial, cardiorespiratory, 
sounds. While it is true that the so-called functional murmurs are 
usually soft and blowing in character, are heard best, as a rule, in the 



CHRONIC VALVULAR DISEASE OF THE HEART 459 

pulmonary area, and are not far transmitted, they often of themselves 
are not distinguishable from organic murmurs; the diagnosis is to be 
based less upon the character of the murmur than upon the concomi- 
tant physical signs, such as hypertrophy of the heart and accentuated 
sounds, on the one hand, and fever, anemia, etc., on the other hand; 
and the disappearance of the murmur with the subsidence of the fever, 
anemia, etc. The cardiorespiratory murmurs are usually heard along 
the left border of the heart, are soft and blowing in character, often 
loudest at the height of inspiration, and disappear when the patient 
stops breathing. In most cases of valvular lesion, in fact, one may elicit 
almost if not quite conclusive evidence of the valvular disorder without 
any attention to the presence or absence of a murmur whatever. 

Mitral Stenosis. — Mitral stenosis occurs in about 16 per cent, of 
the cases of valvular disease, and double mitral disease in about 12 per 
cent., so that mitral obstruction occurs in a total of 28 per cent. 

Etiology. — Mitral stenosis may be due to: (1) Endocarditis, in which 
event it is especially common in adolescents, and young adults, as a sequel 
of rheumatism, "growing pains," chorea, scarlatina, and other infections; 
and (2) slowly progressing sclerosis, analogous to arteriosclerosis, a 
form encountered in later life, and in men as well as in women. In 
many cases, especially in adult women, no etiological factor can be 
determined with certainty — which has led some observers, perhaps too 
frequently, to believe them congenital. Two forms of the disease 
may be distinguished: in the one, found especially in young persons, 
the leaflets, perhaps only slightly thickened, have become adherent 
at their edges, and the chordae tendinese somewhat thickened, short- 
ened and fused, so that the valve viewed from the auricle seems to 
have become converted into a hollow cone — the so-called funnel-shaped 
mitral valve. In the second variety, more common in adults, the leaflets 
are much thickened, indurated, perhaps calcified, and distorted, and are 
represented by a rigid, often atheromatous, mass of tissue exhibiting a 
central linear slit, admitting perhaps only the tip of the little finger — the 
so-called button-hole mitral valve. The mitral ring is often converted 
into a fibrous or calcareous ring, the chordae muscles are shortened and 
thickened, the papillary muscles even may be inserted directly into the 
edge of the leaflets. In both varieties there is practically always an 
associated mitral insufficiency; rarely perhaps in the first-mentioned 
variety, when the leaflets are pliable, there may be a pure mitral stenosis. 
(3) A relative obstruction (or stenosis) is occasionally produced by 
exuberant vegetations, ball-valve thrombus, aneurysmal dilatation 
of the leaflets, etc., and a condition sometimes spoken of as relative 
stenosis ensues when the cavities become much dilated, while the ori- 
ficial ring remains normal or is relatively slightly enlarged. 

Pathological Physiology. — In mitral stenosis the morbid phenomena 
are much like those in mitral insufficiency. There is a similar increase 
in the intra-auricular pressure toward the end of auricular diastole, 
due to the blood from the lungs flowing into an insufficiently emptied 



460 DISEASES OF THE ENDOCARDIUM 

auricle; the consequent dilatation and stretching excite the auricle to 
very vigorous contractions, which become augmented in consequence 
of the obstruction to the discharge of blood. The result is an extraor- 
dinary enlargement (hypertrophy and dilatation) of the left auricle, 
which may attain dimensions three or four times the normal (to 200 c.c. 
or more). Increased intrapulmonary pressure is followed by hyper- 
trophy and dilatation of the right ventricle, which as in mitral insuffi- 
ciency is the efficient factor in maintaining compensation. In some 
cases, for a time at least, the increased power of the left auricle serves 
to supply a normal amount of blood to the left ventricle, which in con- 
sequence presents no noteworthy deviations from the normal. In many 
cases, however, on account of associated mitral insufficiency, the left 
ventricle is somewhat enlarged; in most cases the amount of blood 
supplied to the left ventricle is less than normal, in consequence of which 
it is often said to become reduced in size (this is more apparent than 
real). Perhaps in primary or uncomplicated mitral stenosis the left 
ventricle does lessen in size, but the tendency in this direction is usually 
counteracted by the primary and usually associated mitral insufficiency. 
The final breakdown and the visceral and other consecutive changes 
are similar to those that develop in mitral insufficiency. 

Symptoms. — The disease is not incompatible with many years of life 
and comparative freedom from distress. Symptoms when they do de- 
velop are not to be sharply differentiated from those of mitral insuffi- 
ciency, although they are likely to be more marked or more readily 
provoked. Cyanosis usually is of a higher grade, and often gives rise 
to a peculiar "mitral facies" that of itself suggests the diagnosis; 
dyspnoea is more readily induced by exertion and excitement; hemopty- 
sis is more frequent and more easily provoked; and attacks of bronchitis 
are more prone to develop. Precordial pain and distress is often an 
obstrusive and sometimes an intractable symptom. Recurring endo- 
carditis is quite common, and may be the cause of otherwise inexplicable 
attacks of fever and leukocytosis. The vegetations disintegrating are 
often carried into the circulation and set up embolism in different parts 
of the body, notably in the brain, where they may give rise to aphasia, 
hemiphlegia, etc.; but also elsewhere. Paralysis of the left vocal cord 
(simulating aneurysm) occasionally results from pressure on the recur- 
rent laryngeal nerve by the dilated left auricle. The disorder developing 
in early life may lead to stunting of the bodily growth. Recurring attacks 
of failure of compensation are perhaps more common than in mitral in- 
sufficiency. Compensation usually becomes reestablished, but eventually 
more or less complete failure ensues, and the decompensation phenomena 
mentioned in connection with mitralinsufficiency develop. 

Physical Signs. — The signs of hypertrophy of the right ventricle are 
the same as those in mitral insufficiency (which is often associated and 
presents its own diagnostic signs). In mitral stenosis, perhaps, there 
is more enlargement of the right ventricle; the left auricle also is usually 
more enlarged, and may perhaps present some percussion evidence of 



CHRONIC VALVULAR DISEASE OF THE HEART 461 

this in dulness upward and to the left; but commonly this is not found, 
since the increase in the size of the left auricle is usually predominantly 
anteroposterior. Occasionally there is impaired resonance in the left 
infraclavicular fossa, due perhaps to compression of the lung ^by 
the dilated left auricle; in other cases the enlarged auricle may occa- 
sion some dulness in the left interscapular region. At the apex a 
diastolic or presystolic thrill is commonly palpable, and usually followed 
by, or the thrill ends in, a quick, thumping, or tapping apex beat. The 
murmur of mitral stenosis, which is often limited to a small area near 
the apex, but is not infrequently audible over a considerable area about 
the apex, is diastolic in time; it may occur during any part of the diastole 
or throughout the entire diastole. Perhaps the commonest is the 
interrupted diastolic murmur (so-called Fraentzel murmur), a murmur 
louder at the beginning and the end of diastole than during the mid- 
period (a mid-diastolic diminuendo and presystolic crescendo murmur); 
this is due doubtless to the greater quickness of the flow of blood at the 
beginning of diastole than during the mid-period, and an increased 
acceleration at the end of diastole occasioned by the contraction of the 
auricle. The next most common murmur is the definitely late-diastolic 
(or presystolic) rough, rumbling, crescendo murmur; then a simple 
diastolic murmur, or a continuous murmur occupying the entire diastole 
and the long pause. There may also be a double diastolic tone at the 
apex (bruit de rappel, Bouillard), which under excitement may be 
replaced by a double murmur, or a sound and a murmur. A loud, 
sharp, snappy first sound at the apex is quite characteristic of mitral 
stenosis, and in the absence of a murmur (but associated with the other 
signs) suffices for the diagnosis. It is best explained as due to differences 
greater than the normal in the tension of the mitral leaflets at the begin- 
ning and the end of systole (closure-time). These auscultatory signs 
vary much from time to time, being much influenced by quietness and 
excitement and by strength and weakness of the heart muscle. The 
pulmonary second sound is accentuated or reduplicated. The pulse 
is small and irregular, due to incomplete filling of the ventricle. When 
the heart fails the murmur may disappear (auricular paralysis) and 
the second sound at the apex become inaudible, so that only the loud 
first sound may be heard at the apex; to which, however, are usually 
added the signs of tricuspid regurgitation, and the general evidences of 
failure of the circulation. With restoration of compensation the murmur 
usually again becomes audible, and the pulmonic second sound accent- 
uated. 

Diagnosis. — The characteristic diagnostic signs consist of enlarge- 
ment of the right ventricle (and also of the left auricle, if it can be 
demonstrated), a diastolic or presystolic thrill and murmur at the 
apex, a loud, snappy, first sound at the apex, an accentuated pulmonic 
second sound, and. a small, weak, and irregular pulse. Aortic insuffi- 
ciency accompanied by a presystolic (Flint) murmur is to be dis- 
tinguished, not by the character of the murmur, but by the associated 



462 DISEASES OF THE ENDOCARDIUM 

physical signs. Adherent pericardium, with dilatation of the heart, 
also is sometimes accompanied by a presystolic murmur — which, how- 
ever, rarely if ever has a crescendo character, and is not accompanied 
by the other physical signs of mitral stenosis, but by those of adherent 
pericardium. The presystolic murmur of the very rare tricuspid steno- 
sis will scarcely lead to diagnostic confusion. 

Aortic Insufficiency. — Aortic insufficiency occurs in about 36 per 
cent, of the cases; in about 12 per cent, the lesions are described as 
double aortic disease, and in 18 per cent, there is associated mitral 
valve disease. 

Etiology. — Aortic insufficiency may be due to: (1) Endocarditis. This 
occurs especially in adolescents and young adults, and although un- 
common, is perhaps more common than is generally believed. It may 
be a sequel of rheumatic fever, but is more likely to result from pyococcic, 
pneumococcic, and gonococcic infections. In perhaps a few cases the 
vegetations disappear without permanently damaging the leaflets. 
Usually, however, one or more of the leaflets becomes thickened, indu- 
rated, and curled upon itself, so that the normal approximation during 
diastole is impossible. In a few cases the leaflets become adherent 
to one another at their adjacent edges, so that to insufficiency, stenosis 
is added. Rarely a leaflet may become perforated by the necrosing or 
ulcerative process. (2) Arteriosclerosis. This is the common form. 
Although it occasionally occurs in women, it is especially frequent in 
men after the fortieth year, and is associated with antecedent alcoholism, 
syphilis, and excessive muscular strain, as well as the causative factors 
of arteriosclerosis and high arterial tension. Occasionally following 
syphilis, the disorder may develop in comparatively young men — 
several years after the infection. In later life a so-called parasyphilitic 
form occurs and is rather frequently associated with tabes dorsalis. 
The lesions are those of arteriosclerosis (involving especially the aorta), 
of which the valvular disorder constitutes a part. One or more of the 
valve segments lose their tonicity and plasticity, become indurated, 
curled at their edges and consequently shortened, and are then unable 
to close the orifice. In some cases calcification follows and the segments 
become rigid; or they become adherent at their adjacent edges, so that 
to the insufficiency stenosis is added; but stenosis is much less common 
than is usually thought. (3) Rarely the disorder may be traumatic, 
developing in consequence of sudden undue muscular strain, severe 
contusions or compression of the chest, etc., which lead directly to rup- 
ture of usually a single leaflet (normal or previously diseased). (4) 
Relative insufficiency rarely ensues in consequence of dilatation of the 
aortic ring, due to loss of elasticity, and associated with considerable 
dilatation of the arch of the aorta. (5) In a few cases the condition is 
congenital, due to fusion or other malformation of the leaflets. 

Pathological Physiology. — In consequence of incompetency of the 
aortic valve the left ventricle during diastole receives blood from two 
sources — the normal volume from the left auricle and a variable amount, 



CHRONIC VALVULAR DISEASE OF THE HEART 463 

the regurgitating stream, from the aorta. Whether the regurgitating 
stream is considerable in amount, and gradually increases with the 
progress of the disorder, as is generally believed, or is only a relatively 
small amount of the total volume of ventricular blood, as the recent 
researches of Stewart suggest, the fact is that the intraventricular dias- 
tolic pressure becomes increased. The tension and stretching to which 
the ventricular musculature is thus subjected stimulate it to vigorous 
contractions, in an effort to expel the augmented amount of blood, and 
the constant recurrence of the stimulus ultimately induces more or 
less hypertrophy. The enlargement of the cavity of the ventricle (dila- 
tation) and the concomitant hypertrophy may and usually do counter- 
balance each other, so that for a considerable period the periphery is 
sufficiently supplied with blood and the patient suffers no noteworthy 
ill consequences. Ultimately the heart may reach enormous proportions, 
the largest seen (bovine heart), and may weigh 1200 grams or more. 
In the course of time dilatation assumes the ascendency over the hyper- 
trophy in consequence of deficient blood supply through the coronary 
circulation (narrowing of the coronary orifices and sclerosis of the vessels 
in their course) and concomitant myocardial degeneration; the equi- 
librium of the circulation is no longer maintained and failure of compen- 
sation ensues. The gradual enlargement of the ventricular cavity leads 
to relative mitral insufficiency, and this in turn to its own ill effects, 
already mentioned; organic mitral insufficiency also may occur. The 
aorta, especially the ascending arch, is usually considerably dilated 
(so-called fusiform aneurysm), but it may be only unusually distensible; 
that is, there are signs of enlargement during life (expansion due to the 
systolic output of a large volume of blood), but no material increase 
in size after death (so-called dynamic dilatation). The systolic output 
of a large volume of blood is also apparent in the violent throbbing of 
the superficial arteries, which, as the result of the long continued strain 
to which they are subjected, usually reveal more or less sclerosis (which 
may be due also to other factors — alcoholism, syphilis, plumbism, etc.). 
In the acute cases that develop suddenly in consequence of rupture or 
rapid destruction of a leaflet, compensation cannot be immediately 
effected, and the patient suffers immediate distress. An old sclerotic 
valve may become the seat of acute endocarditis. 

Symptoms. — Well compensated aortic insufficiency may be disclosed 
only by a physical examination of the heart; indeed, in many cases the 
disorder is for a long time overlooked on account of the absence of 
subjective symptoms, the slight degree of hypertrophy of the left ventricle, 
and the softness or indistinctness of the murmur. In many cases the 
earliest symptoms consist of dizziness, perhaps amounting almost to 
faintness, throbbing headache, flashes of light before the eyes, tinnitus 
aurium, muscular weakness, and palpitation of the heart and dyspnoea 
on sudden exertion. The phenomena, which, as a rule, rapidly subside 
upon the restoration of quiet, are attributable to cerebral anemia. 
Marked pallor (aortic facies) and a readily induced flush are usually 



464 DISEASES OF THE ENDOCARDIUM 

conspicuous symptoms; the flush may be accompanied or followed by 
sweating, which with occasional hemoptyses has suggested tubercu- 
losis to the unwary; there may also be slight oedema due to the anemia. 
Precordial pain is often present and sometimes distressing; it is usually 
dull and aching, but may be severe and sharp and radiate to the neck 
or arms (especially the left). True angina pectoris also occurs; more 
frequently in aortic insufficiency than in any other form of valvular 
disease. 

As compensation fails the aforementioned symptoms become per- 
sistent and aggravated: cough, dyspnoea, and palpitation of the heart 
in a rather pallid subject are quite characteristic. With the advent 
of relative mitral insufficiency the symptoms of this condition may 
supervene; but cyanosis is rarely marked, hemoptysis is not common, 
and oedema is not extreme or widespread, being usually limited to the 
feet and ankles and other dependent parts of the body. Embolic phe- 
nomena are not uncommon— in the brain, spleen, kidneys, etc. Nervous 
symptoms are often obtrusive — irritability, restlessness, insomnia, 
melancholia, delusions, suicidal tendencies, etc. For a long time com- 
pensation may be unstable, and although when more or less lost it 
may sometimes be restored, the restoration is much less readily effected 
than in any other form of valvular disease; this decompensation, espe- 
cially in elderly subjects, often betokens the final lethal termination. 
Sudden death is not uncommon, being often due to blockage of the 
coronary arteries. 

In the acute cases that develop from rupture (traumatism or ulcerative 
processes), dyspnoea, precordial pain, palpitation of the heart, some- 
times hemoptysis, etc., often come on immediately and may prove 
extremely distressing, until the heart finally more or less effectually 
compensates the lesion. 

Physical Signs .—Depending upon the youth of the subject when the 
disorder developed and the degree of hypertrophy of the left ventricle, 
there is more or less bulging of the precordium; the cardiac impulse 
is forcible and widespread, and the apex beat (the palpable beat farthest 
downward and outward) is displaced to the sixth, seventh, or eighth 
intercostal space outside the mamillary line to the anterior or mid- 
axillary line; it is usually strong and forcible and heaving in character, 
and, considering the size of the heart, is rather pointed (in contrast to the 
much wider and rounded apex of hypertrophy of the right ventricle). 
Visible and forcible pulsation of the arteries is present during compen- 
sation and is quite significant of aortic insufficiency; it is especially ob- 
vious in the aorta (episternal notch and perhaps the second right inter- 
costal space), the carotids, temporals, retinals, subclavians, brachials, 
radials, femorals, and often the small arteries of the hands and feet. The 
pulsations may be so forcible as to occasion a visible nod of the head 
with each heart beat (Musset's sign) and a jerk to a leg crossed over 
the other feg. In cases of marked elongation and tortuosity of the 
arteries, the pulsations are peculiarly serpentine, and were interpreted 



CHRONIC VALVULAR DISEASE OF THE HEART 465 

by an alcoholic patient of mine as certain evidence of snake invasion. 
Usually the pulsation is transmitted to the capillary vessels, and may be 
apparent upon mere inspection of the face or hands, or the oral mucous 
membrane (uvula, for instance); or it may be readily brought in evidence 
by rubbing the skin for a moment, or by slight pressure on a finger nail, 
or on the lip mucous membrane by a glass slide. This is significant 
but not diagnostic of aortic insufficiency, since it may be found also in 
other conditions of relaxation of the peripheral arteries (in health as 
well as in disease). In a few cases there may be an arterial pulsation 
in the liver. In a few cases the pulsations are still further transmitted — 
into the small veins, especially of the back of the hands (the penetrating 
or centripetal pulse of Quincke). The arterial pulse on palpation is 
quite characteristic — of increased volume and force, sudden of impact 
and of fall, and is empty between beats — the so-called Corrigan, water- 
hammer, pistol, or receding pulse; pulsus altus et celer. Usually it may 
be well perceived by grasping the muscle of the forearm in the hand. 
The sudden collapse is usually attributed to diastolic regurgitation of 
a large volume of the blood through the incompetent aortic valve, but 
it is more likely due in large measure to reflex dilatation of the peripheral 
arterioles, induced by stimulation of the ventricular wall in consequence 
of increased pressure (Stewart); and to this also is due the capillary 
pulse and the penetrating venous pulse. Stewart interprets this periph- 
eral vascular relaxation as a means of preventing the ill effects of 
undue pressure on the ventricle. A diastolic thrill is sometimes palpable 
at the base, near or beneath the sternum; rarely it may be felt also at 
the apex; occasionally a thrill at the apex is presystolic (analogous to 
the Flint murmur); in many cases there is a double thrill at the base, 
the systolic element being well transmitted into the aorta and the 
carotids; this is by no means always due to associated aortic stenosis. 
On percussion there is increase of the cardiac dulness diagonally, in 
the direction of the long axis of the heart. The area of dulness becomes 
diagonally ovoid, downward and to the left; only in advanced cases 
with consecutive dilatation and relative mitral insufficiency does the dul- 
ness become much increased to the right. The characteristic murmur 
is diastolic in time, soft and blowing in character, beginning with dias- 
tole and gradually decreasing in intensity; it is heard best usually (but 
not always) over the middle or at the left edge of the sternum on a level 
with the third rib, and it is transmitted down the left edge of the sternum 
to the ensiform cartilage, or to the apex (where it may be quite as loud 
as at the base of the heart), or to the axilla (apart from its transmission 
to the apex). Sometimes the murmur is so faint as to be almost if not 
quite inaudible; it may be harsh and rasping, or musical. In most cases 
there is a double murmur in the aortic area (the to-and-fro bellows 
murmur of Stokes) — the diastolic murmur already mentioned, and a 
systolic murmur often harsh in character, and transmitted into the 
carotids; it is due to roughening of the aortic leaflets, sclerosis of the 
aorta, dilatation (fusiform aneurysm) of the aorta, aortic stenosis (rare), 
30 



466 DISEASES OF THE ENDOCARDIUM 

true aneurysm, or the impact of the regurgitating with the outgoing 
stream of blood. In many cases (25 to 50 per cent.) a presystolic (Flint) 
murmur, quite like that of mitral stenosis, is audible at the apex; it is 
probably due to the regurgitating stream of blood impinging upon and 
actually driving the anterior mitral leaflet toward the centre of the ven- 
tricle, thus interfering with the entrance of blood into the ventricle at the 
time of auricular systole by producing essentially a moderate mitral 
stenosis (Guiteras); or to vibrations of the anterior mitral leaflet between 
the two streams of blood. The aortic second sound is usually wholly, 
occasionally only partly, replaced by the diastolic murmur (perhaps the 
lesion is less serious when the sound is only partly replaced). The 
systolic murmur (sometimes both murmurs) is more or less well trans- 
mitted to the subclavian, axillary, and carotid arteries. A rather loud, 
sharp, systolic (vascular diastolic) sound (pistol-shot sound) is some- 
times audible over the larger arteries, especially the femorals; it is pro- 
duced locally and is not transmitted from the heart. Rarely two sounds 
may be heard, the second coincident with the collapse of the artery 
(Traube's sign). Pressure with a stethoscope on the femoral artery, in 
addition to a systolic murmur thus normally produced, sometimes results 
in the production of a cardiac diastolic murmur (Durosiez's sign). Sys- 
tolic contraction of the pupil (due to elongation of the vessels of the 
iris) and diastolic dilatation (lessened amount of blood) may be observed 
(Landolfi's sign). 

With the development of myocardial weakness, dilatation of the heart, 
relative mitral insufficiency, etc., the physical significance of these dis- 
orders also develop. 

Diagnosis. — The characteristic diagnostic signs consist of evidences of 
enlargement of the left ventricle, a diastolic murmur at the base of the 
heart transmitted down the sternum, toward the apex beat, or into the 
axilla, marked visible pulsations of the superficial arteries, the Corrigan 
pulse, a capillary pulse, and Traube's and Durosiez's signs. The 
murmur is often very faint or quite inaudible, in which event the diag- 
nosis may be quite apparent from the hypertrophy of the left ventricle, 
the collapsing pulse, and the pallor of the patient. The commonly 
associated systolic murmur in the aortic area should be correctly inter- 
preted; usually it does not mean aortic stenosis. The presystolic (Flint) 
murmur at the apex is to be distinguished from the similar murmur of 
mitral stenosis by the associated signs, especially the presence of hyper- 
trophy of the left rather than the right ventricle, absence of accentuation 
of the pulmonic second sound, the presence of arteriosclerosis, and the 
character of the pulse. It is scarcely likely that the rare inorganic 
diastolic murmurs, or those due to pulmonary insufficiency, will lead 
to diagnostic confusion. Evidences of fusiform dilatation of the aorta 
must not be mistaken for true aneurysm. 

Aortic Stenosis. — Aortic stenosis alone occurs perhaps in 1 to 2 per cent, 
of the cases of valvular disease; in about 12 per cent, of the cases the 
condition is described as double aortic disease (insufficiency and stenosis) . 



CHRONIC VALVULAR DISEASE OF THE HEART 467 

Etiology. — Aortic stenosis may be due to: (1) Endocarditis. This 
is quite rare, but may follow rheumatism and other infections, and occurs 
in young subjects. In consequence of organization of the vegetations, 
the leaflets become thickened, indurated, and adherent at their adjacent 
margins, so that varying grades of obstruction ensue. Later a deposit of 
lime salts may occur, so that the leaflets with the aortic ring may form 
a dense calcified mass of tissue with a variable sized and shaped opening. 
(2) Arteriosclerosis. This is the common form of aortic stenosis; but 
in itself it is rare, and is always part of general arteriosclerosis, especially 
of the aorta. It occurs, therefore, especially in elderly subjects. The 
process is slow, although usually progressive, and ultimately leads to 
thickness and marked, often cartilaginous, rigidity of the leaflets, 
with corresponding obstruction to the blood curent. In advanced cases 
there is usually considerable calcareous infiltration, in which event the 
lesions are much like those mentioned in connection with the endocarditic 
form. (3) Relative aortic stenosis (a misnomer) is a term sometimes 
used to designate that condition in which, with normal aortic leaflets 
and aortic ring, the aorta just beyond is unusually dilated. (4) There 
are other rare types: fusion and thinning of the leaflets — perhaps congen- 
ital; fibrocalcareous thickening and induration of the aortic ring without 
involvement of the leaflets; a subvalvular constriction involving the 
mitrosigmoidian sinus and probably due to foetal endocarditis, etc. 

Pathological Physiology. — On account of obstruction at the aortic ori- 
fice, the left ventricle is unable to expel the normal amount of blood in 
the normal time. In consequence, a residual amount of blood is present 
in the ventricle at the beginning of diastole, which, with the normal 
amount received from the auricle, leads to increased intraventricular 
pressure; this, together with stimuli occasioned by resistance at the 
aortic orifice to be overcome, induces hypertrophy of the left ventricle 
— which is the effective factor in maintaining compensation, although 
it never attains the dimensions of that of aortic insufficiency. This 
hypertrophy is often sufficient to enable the heart to propel the normal 
amount of blood into the aorta; no noteworthy dilatation ensues, and 
the patient suffers no ill consequences. The systole, however, is pro- 
longed. When the stenosis becomes greater than can be compensated 
by hypertrophy of the left ventricle, or when the myocardium becomes 
enfeebled in consequence of insufficient nourishment (coronary sclerosis), 
dilatation ensues, and ultimately perhaps relative mitral insufficiency and 
its consequences. 

Symptoms. — Well compensated aortic stenosis is often for a long time 
latent. Symptoms when they develop are much like those of aortic 
insufficiency, which is usually associated; with absence of aortic insuffi- 
ciency the symptoms are likely to be less severe, although perhaps 
readily induced by exertion. When dilatation ensues, the symptoms 
of failing compensation and relative mitral insufficiency develop. 

Physical Signs. — In young subjects there may be bulging of the pre- 
cordium due to hypertrophy; but since the hypertrophy is often slight, 



468 DISEASES OF THE ENDOCARDIUM 

for a long time it may be overlooked, especially in elderly emphysematous 
subjects. The signs of hypertrophy when apparent are analogous to 
those mentioned in connection with aortic insufficiency, although less 
marked. Usually there is a rough systolic thrill at the aortic cartilage 
propagated into the aorta and the carotid, perhaps other nearby arteries. 
The pulse is quite characteristic: it is small or moderate in volume, 
slow (pulsus tardus), and rises slowly (prolonged systole), is well sus- 
tained (broad summit), and falls slowly. On auscultation there is a 
systolic murmur at the base of the heart, which obscures or replaces the 
first sound and is usually rough and rasping in character, sometimes 
loud and musical (perhaps audible at a distance), but may be soft 
(especially when the ventricle is weak); its point of maximum intensity 
is at or near the aortic cartilage, and it is usually transmitted to the 
carotid arteries, and sometimes to the descending aorta (audible in the 
left interscapular space), the axillary arteries, etc. Occasionally it is very 
loud at the apex (without any associated mitral insufficiency). The 
second aortic sound is commonly absent or weak, or replaced by a dias- 
tolic murmur, on account of rigidity of the aortic leaflets and commonly 
co-existing aortic insufficiency. With the advent of myocardial weakness 
and dilatation, relative mitral insufficiency usually ensues and materially 
modifies the previously existing physical signs. 

Diagnosis. — The characteristic diagnostic signs consist of evidences 
of enlargement of the left ventricle, a systolic thrill and a systolic murmur 
at the base of the heart and transmitted into the aorta and carotid 
arteries, a weak or absent aortic second sound, and a slow (as distin- 
guished from an infrequent) pulse. A basal systolic murmur, upon which 
the diagnosis is often based, is usually due to some other disorder, such 
as roughening of the aortic leaflets, sclerosis of the aorta, dilatation (fusi- 
form aneurysm) of the aorta, true aneurysm, or the impact of a regurgi- 
tating with the outgoing stream of blood. Sclerosis or atheroma of the 
aorta may be differentiated by absence of the characteristic pulse and 
usually also of a thrill, and the presence of an accentuated aortic second 
sound and of other signs of arteriosclerosis. Dilatation of the aorta and 
true aneurysm may be recognized by their own diagnostic signs. The 
basal systolic murmurs of anemia, fever states, etc., usually have an 
obvious cause, are rarely loudest in the aortic area, and do not give 
rise to enlargement of the left ventricle. Pulmonary stenosis and mitral 
insufficiency, which perhaps might enter into the diagnosis, give rise to 
enlargement of the right rather than the left ventricle, and other 
unequivocal signs. 

Tricuspid Insufficiency. — Etiology. — Tricuspid insufficiency rarely 
results from acute or chronic endocarditis (antenatal or postnatal). 
Usually the condition is relative and due to inability of the muscle of 
the right heart to perform the work to which it is subjected. This 
insufficiency, especially as a temporary disorder, is much more common 
than is suspected; it develops in health under the stress of unusual or 
sudden strain (athletic exercises, parturition, etc.), and in disease when 



CHRONIC VALVULAR DISEASE OF THE HEART 469 

the enfeebled myocardium is suddenly called upon for some extra 
work — in both of which circumstances the safety-valve action of the 
right ventricle (involving the wall of the ventricle, the papillary mus- 
cles, which readily become fatigued and act imperfectly or ineffectually, 
and the tricuspid ring) becomes operative and prevents serious and 
lasting damage to the myocardium. The more obvious and clinically 
important tricuspid insufficiency occurs in chronic hypertrophy with 
consecutive dilatation of the right ventricle, which in turn results from 
advanced mitral valve disease, chronic diseases of the lungs (emphysema, 
bronchitis, interstitial pneumonitis, pleural adhesions, etc.), pericardial 
adhesions, and myocardial weakening due to any local or general cause. 
There is associated congestion of the liver, spleen, kidneys, gastro- 
intestinal tract, etc., oedema of the subcutaneous tissues, effusions in the 
serous sacs, etc. 

Symptoms. — The symptoms are those of failing cardiac compensation 
and are due to the associated passive congestion and consequent func- 
tional inactivity of the organs. The embarrassment of the heart itself is 
obvious in precordial distress or pain and palpitation of the heart. Con- 
gestion of the lungs leads to cyanosis, dyspnoea (aggravated upon exer- 
tion and excitement), cough, expectoration, hemoptysis, etc.; of the 
liver, to local pain and tenderness; of the gastro-intestinal tract, to poor 
appetite, disordered digestion, flatulence, nausea, vomiting, consti- 
pation, etc.; of the kidneys, to oliguria, albuminuria, cylindruria, 
erythrocyturia, etc. (Edema is always present and may become universal; 
effusions are common in the serous sacs, especially the right pleura; 
ascites is rarely present before general oedema, but it may be dispropor- 
tionately marked. 

Physical Signs. — The physical signs consist of dilatation of the heart, 
especially of the right side (the dulness may extend to the right nipple 
line) ; a systolic murmur (usually soft and blowing, but sometimes rough) 
in the tricuspid area (and especially significant if heard to the right of 
the sternum, where the murmur of mitral insufficiency is rarely heard); 
a ventricular systolic autochthonous pulsation in the veins of the neck, 
often especially marked in the jugular bulb and sometimes propagated to 
adjacent veins (rarely a murmur may be heard); and a ventricular 
systolic expansile pulsation of the liver. The signs of the antecedent 
disorder, usually mitral valve disease, or chronic disease of the lungs, etc., 
are also present. Enfeeblement of a previously accentuated pulmonic 
second sound is a valuable sign of the development of tricuspid insuffi- 
ciency; as the insufficiency grows less (or the right side of the heart 
grows stronger) the pulmonary second sound again becomes accentuated. 
The safety valve leakage usually occasions no noteworthy symptoms 
and soon subsides; indeed, the occurrence of the leakage probably 
prevents the onset of more or less serious symptoms. 

Tricuspid Stenosis. — Etiology. — Tricuspid stenosis is a rather rare 
condition. It may be due to endocarditis, either antenatal or postnatal 
(usually rheumatic); rarely it seems to be primarily degenerative, analo- 



470 DISEASES OF THE ENDOCARDIUM 

gous to the arteriosclerotic process. It is most common in women 
(75 per cent, of the cases), and in more than 99 per cent, of the cases 
is associated with disease of one or more of the other valves, especially 
mitral stenosis (56 per cent, of the cases). The characteristic lesions 
consist of hypertrophy and dilatation of the right auricle. 

Symptoms. — The symptoms are virtually those of mitral stenosis. 
Cyanosis is often the earliest obtrusive symptom, and may be present 
for months before there are other noteworthy manifestations of de- 
compensation. Polycythemia is common and the fingers may be clubbed. 
When the heart begins to fail, the symptoms cannot be distinguished 
from those of tricuspid insufficiency. Dropsy may occur early and is 
unusually persistent. 

Physical Signs. — The physical signs are commingled with those of the 
complicating lesions; but the significant signs consist of increase of the 
cardiac dulness to the right (which may extend to or beyond the mammil- 
lary line); a presystolic or diastolic thrill, and a usually rough, rumbling 
presystolic or diastolic murmur, sometimes ending in a rather sharp 
first sound, at the end of the sternum; and presystolic (auricular systolic) 
pulsations in the veins of the neck and in the liver. 

Pulmonary Insufficiency. — Etiology. — Pulmonary insufficiency is very 
rare as an acquired affection, but it sometimes results from acute 
endocarditis (usually set up by the pyococci, sometimes by the gono- 
coccus). Occasionally in cases of long-standing high pulmonary tension 
there is some sclerosis of the leaflets and consequent insufficiency. 
Perhaps relative insufficiency sometimes results from stretching of the 
pulmonary ring in conditions of high pulmonary pressure. The lesions 
much resemble the analogous lesions of aortic insufficiency, involving, 
however, the right instead of the left ventricle. 

Symptoms. — Symptoms are in abeyance until the right heart begins 
to fail, whereupon the phenomena common in decompensation develop. 
Physical Signs. — The physical signs consist of hypertrophy and later 
of dilatation of the right ventricle, and a diastolic murmur at the base of 
the heart, usually loudest in the pulmonary region and transmitted down 
the left edge of the sternum. Aortic insufficiency may be excluded by 
the absence of enlargement of the left ventricle and of the characteristic 
vascular phenomena. 

Pulmonary Stenosis. — Etiology. — Acquired pulmonary stenosis is 
the rarest of valvular lesions. Occasionally it follows acute endocarditis, 
or the endocarditis may become engrafted upon an old, perhaps con- 
genital defect; occasionally also the lesion may be due to slow sclerosis, 
when it is associated with pulmonary endarteritis. Very rarely, perhaps 
trauma may lead to rupture of one of the leaflets. The lesions are much 
like the analogous aortic stenosis, involving, however, the right instead 
of the left ventricle. 

Symptoms. — Symptoms are not obtrusive until the right heart begins 
to fail, whereupon the symptoms common to decompensation ensue. 



CHRONIC VALVULAR DISEASE OF THE HEART 471 

Physical Signs. — The physical signs consist of hypertrophy and 
dilatation of the right ventricle, a systolic thrill and murmur in the 
pulmonary area, and a weak or absent pulmonary second sound; or the 
sound may be replaced by a diastolic murmur. A systolic murmur 
is very common in the pulmonary region, but it is rarely due to pulmonary 
stenosis: it may occur in healthy, thin-chested persons, especially chil- 
dren, and is often induced by exercise; it is common in anemic, cachectic, 
and fever states; it may be due to the interaction of the heart and the 
lung (cardiopulmonary murmur); and it may be due to aortic stenosis 
(and the other factors mentioned as causative of an aortic systolic 
murmur), or to mitral insufficiency. In most of these cases the diagnostic 
inference is obvious: aortic stenosis may be excluded by absence of 
hypertrophy of the left ventricle, of propagation of the thrill and murmur 
into the carotid arteries, and of the characteristic pulse. Mitral in- 
sufficiency may be excluded by the absence of the common signs, espe- 
cially the accentuated pulmonary second sound. 

Combined Valvular Lesions. — In almost, if not quite, one half of 
the cases of valvular disease, there is more than a single lesion; that is, 
there may be insufficiency and stenosis at one valve, or two or more 
valves may be diseased. This double or multiple involvement of the 
valves may develop at the one time, or, what is more common, involve- 
ment of one valve follows that of another; and the lesions may be alike 
in nature or dissimilar. Thus, while rheumatic and other infections 
commonly involve only the mitral valve, they not infrequently at or 
about the same time, especially in children, involve also the aortic valve, 
and occasionally also one or both valves of the right side of the heart. 
More commonly, however, the primary lesion, usually insufficiency, 
is followed in the course of time by cicatrization and consequent stenosis : 
thus mitral insufficiency often in the course of time becomes associated 
with stenosis (so-called double mitral disease); mitral stenosis is rare 
as a single lesion, being usually associated with insufficiency; aortic 
insufficiency is often the primary and may remain the only lesion, but 
sometimes becomes associated with stenosis (double aortic disease); 
aortic stenosis as a single lesion is the rarest of all in the left side of the 
heart. The developing stenosis may for a time at least prove beneficial 
in lessening the primary insufficiency and retarding the development 
of its ill effects. Varying combinations of aortic and mitral valve disease 
also occur, especially aortic and mitral insufficiency, due usually to 
sclerosis rather than to endocarditis. The commonest combination of 
valvular disorders, however, is that of an organic lesion at one orifice, 
followed by relative insufficiency at another: mitral insufficiency or 
stenosis followed by tricuspid insufficiency, and aortic insufficiency or 
stenosis followed by relative mitral insufficiency and later relative 
tricuspid insufficiency. 

Physical Signs. — Associated valvular lesions materially alter the 
physical signs of individual lesions and proportionately increase the 
diagnostic difficulties. In the diagnosis accuracy will be best achieved by 



472 DISEASES OF THE ENDOCARDIUM 

paying less attention to the murmurs than to the other physical signs, 
and by postulating the fewest defects compatible with an explanation 
of the recognizable physical signs. A systolic murmur alone is of no 
value whatever in the diagnosis; a diastolic murmur almost certainly 
means a valvular defect, but in this event there are always corroborative 
signs. The loudest, most obtrusive murmur (usually systolic) may be 
due to a secondary lesion (relative insufficiency), the murmur of the 
primary lesion being soft or almost inaudible, but in this event also 
the concomitant physical signs correctly determined point the way to 
the correct interpretation of the phenomena. 

Diagnosis. — The diagnostic criteria of the different forms of valvular 
disease have been sufficiently dwelt upon. But the diagnosis is by no 
means complete with the naming of the valvular defect; it must be much 
more comprehensive, and should include the nature of the valvular 
disorder (whether endocarditic, sclerotic, or relative; obsolete or active), 
the degree and adequacy (stability) of the compensating mechanism, 
and the factors that tend to or actually provoke decompensation in the 
individual case; in other words, in addition to ascertaining the valvular 
defect one must determine also the functional capacity of the myocardium 
— the relative preponderance of hypertrophy or dilatation, and the ability 
of the heart to do a measured amount of work without subjective or 
objective distress. 

Prognosis. — The prognosis in valvular disease of the heart depends 
in part upon the nature and severity of the valvular defect, but in large 
measure upon the ability of the myocardium to effect and maintain 
compensation, which in turn is much dependent upon the patient's 
general health and mode of life. The anatomical valvular defects, 
of course, cannot be cured, although material benefit often follows the 
supervention of stenosis upon a well-marked insufficiency; relative 
defects (insufficiencies) due to stretching of orifices may entirely dis- 
appear if the affected orifices regain their normal tone. The anatomical 
defects, however, are not incompatible with long life and more or less 
freedom from distress. In point of gravity, the mitral lesions are less 
serious than the aortic, the order from the least to the most serious being, 
mitral insufficiency, mitral stenosis, aortic stenosis, and aortic insuffi- 
ciency. The cases associated with extensive arteriosclerosis (usually 
aortic insufficiency) are more grave than those the result of past rheu- 
matism, since there is usually also sclerosis of the coronary arteries 
with its attendant danger of angina pectoris, thrombosis and embolism 
of the coronary vessels, and consequent sudden death, etc. In the aortic 
cases also compensation, when once disturbed, is much less readily 
restored than in the mitral cases, and when restored it is usually unstable. 
Double or triple valvular defects, whether organic or relative, add 
materially to the gravity of the prognosis. In children the prognosis is 
generally bad; in women it is better than in men, because of their quieter 
life, the preponderance of mitral lesions, and their less addiction to the 
vices of intemperance, venery, and hard manual labor. Pregnancy, 



CHRONIC VALVULAR DISEASE OF THE HEART 473 

however, adds materially to the gravity of the condition, although a 
considerable number of cardiopaths bear and rear large families. In 
mitral cases there is rarely associated pulmonary tuberculosis (due to 
relative immunity afforded by chronic passive congestion). 

Treatment. — It seems quite likely, although difficult to prove, that 
chronic valvular disease of the heart may be prevented in some cases, 
or that its serious consequences may be lessened or retarded. Since 
most of the cases of the endocarditic group are due to rheumatism, the 
prompt and efficient jugulation of this infection should tend to minimize 
its complications : that this really occurs there can be no doubt, although 
from the nature of the disorder definite proof can scarcely be adduced. 
Since the cases of the sclerotic group are associated with arteriosclerosis, 
and since arteriosclerosis is largely the penalty of unwise living and 
divers sorts of indiscretions, it is quite probable that a rational and 
hygienic mode of life, tending to retard the degenerative changes of 
the arteries, should tend also to prevent the development of many cases 
of chronic degenerative or atheromatous valvular disease. In most of 
these cases, however, "when we have prescribed that continual temper- 
ance in all things which is necessary to the care of most disorders, how 
often do we find that our patient reckons the loss of pain to be purchased 
too dear by the loss of pleasure." (Gee.) 

The chronic valvular disease being a fact, the treatment varies with its 
stage. During the period of compensation, the one important desider- 
atum is so to regulate the patient's life that his activities may be well 
within the potentialities of his myocardium. This may be estimated 
by determining the relative amount of hypertrophy and of dilatation, 
the reaction of the heart and blood vessels to a measured amount of 
work (such as walking, climbing stairs, lifting weights, etc.), and by 
the condition of the other organs (passive congestion, etc.). In most 
cases it is wise to explain to the patient the condition of his heart and 
blood vessels; to tell him that although disabled (impaired), his heart 
is still capable of many years of effective work, provided the demands 
made upon it are well within its reserve power, but that this reserve 
power is less than in normal subjects. The patient's entire life, his diet, 
his work, his rest, his exercise, must be adjusted to the capabilities of his 
heart. The diet should be nutritious and readily digestible; the total 
amount at each meal should not be voluminous, fluids especially being 
restricted and taken between meals; a large meal, as a rule, should not 
be taken in the evening; strict attention should be paid to free daily 
evacuation of the bowels, and to free action of the skin (bathing). The 
patient should have an abundance of rest, and should be as much as 
possible in the open air; his occupation should not be too engrossing 
mentally nor too strenuous physically; and his exercise should be such as 
to afford pleasure, but not to provoke any manifestations of cardiac 
embarrassment. If, on the one hand, the desirable life entails continued 
repression of bodily spirits and intellectual ambitions, it has its com- 
pensation in prolonged life and postponement of the inevitable. It 



474 DISEASES OF THE ENDOCARDIUM 

is especially important to bear constantly in mind that a cardiac murmur 
is no indication whatever for the administration of cardiac tonics (such 
as digitalis); and that therapeutically a murmur is the least important of 
the physical signs. Furthermore, many symptoms, such as attacks 
of precordial distress, palpitation of the heart, dyspnoea, etc., are due 
to causes that excite these symptoms in non-cardiac subjects, such as 
dietetic indiscretions, the abuse of alcohol, tea, coffee, or tobacco, 
excessive venery, worry, anxiety, hill climbing, etc.; and they are to be 
combated by eradication of their cause, rather than by the immediate 
resort to digitalis and similar drugs. In some cases subjective complaints 
of precordial distress and palpitation are found to be associated with an 
excited overhypertrophied heart; the use of digitalis only adds to the 
patient's discomfort, which may be materially lessened by minute doses 
of aconite, small doses of the bromides, valerian, regulation (lessening) 
of the diet, and free purgation. When the disease has advanced and 
the compensation tends to become somewhat unstable (lessened reserve 
power), beneficial results may attend the judicious combination of rest, 
graduated exercises, hydrotherapy, small doses of digitalis or strophanthus 
for short periods, and free purgation. In other cases the imminence of 
decompensation is suggested by anemia and general failure of health, 
and it often yields to iron, quinine, arsenic, strychnine, etc. 

Finally, in some cases suddenly, in most cases gradually, more or 
less complete failure of compensation ensues; the indications to be met 
are to reduce the work demanded of the heart and to increase the strength 
and vigor of its contractions. The most important is, temporarily at 
least, to reduce the work demanded of the heart — which is best effected 
by eradication of the cause (excessive mental or physical work, worry, 
anxiety, excitement, dietetic and other indiscretions, malnutrition, etc.) 
sometimes directly responsible for the breakdown, by rest in bed, regu- 
lation of the diet, and depletion of the engorged venous system. The 
rest in bed should be absolute; nothing else is so important or so effica- 
cious. Rest in bed for ten days or two weeks of itself often suffices 
to restore compensation so seriously disturbed as to lead to considerable 
oedema; with recurring breaks in compensation rest in bed may continue 
to suffice, in which event digitalis and other cardiac tonics need not be 
given; they should be reserved until needed — which assuredly tends to 
prolong the patient's life. The diet should be carefully regulated to suit 
each individual patient, the main indications being to nourish the patient 
(concentrated, readily digestible, solid and semisolid foods), to prevent 
flatulence (avoidance of food likely to undergo fermentation), and to 
limit the amount of fluid intake (which not only overloads the blood 
and adds to the work of the heart, but also distends the stomach and 
mechanically adds to the embarrassment of the heart). The digestive 
processes may be much improved by free purgation by blue mass (or 
calomel) and salines, which serve to deplete the engorged gastrointes- 
tinal and hepatic systems. 

In many cases the foregoing do not suffice, or, having once or twice 



Chronic valvular disease of the heart 475 

proved efficacious, they are inadequate in a later recurrence of decom- 
pensation ; recourse must be had to drugs that increase the strength and 
vigor of the cardiac contractions. Digitalis is the sovereign remedy. 
Since it increases the tonicity, contractility, excitability, and rhythmi- 
city of the cardiac muscle, it is indicated in the failure of compensation 
that may develop in any and all forms of valvular disease. The special 
indication for its use is insufficiency (dilatation) of the myocardium, 
manifested by cyanosis, dyspnoea, venous stasis, and oedema, rather 
than any special valvular defect per se. The best effects of the drug 
are seen in cases of dilatation with final tricuspid insufficiency, congestion 
of the viscera, and oedema. In appropriate cases, its good influences are 
obvious often within twenty-four hours : the volume of the heart lessens ; 
the cardiac action becomes regular and vigorous; the pulse becomes 
full, strong, and regular; dyspnoea, cyanosis, and cardiac palpitation 
lessen; the urine increases in amount; and the oedema begins to be ab- 
sorbed. It is no less efficacious in aortic insufficiency with dilatation 
and venous congestion than it is in mitral valve disease; the theoretical 
objection to its use in aortic insufficiency, based upon its prolonging the 
ventricular diastole, is more than counterbalanced by its action in pro- 
moting a full, vigorous, and efficient systole with complete emptying of 
the ventricle, in raising the tension in the systemic arteries, and in 
leading to the establishment of circulatory equilibrium in the capillaries 
and veins. 

There are three good preparations — the powdered leaves, the infusion, 
and the tincture; the infusion is perhaps the best, but must always be 
freshly prepared from the leaves. It may be serviceably combined with 
alkaline diuretics : 

I$i — Potassium acetate, 

Potassium citrate, of each 2 drams 8|0 

Infusion of digitalis 6 ounces 200 lo 

M. S.- — One tablespoonful (15 c.c.) every four hours (or at longer intervals, as may be 
required). 

Failure in the use of digitalis is attributable to inefficient preparations 
made from inert leaves (or the preparation of a supposed infusion from 
a mother fluid extract or similar preparation), insufficient dosage, and 
unsuitable case. When the stomach is or becomes deranged (nausea, 
vomiting, etc.), a fat-free tincture may be employed, or the infusion may 
be given by the rectum; or digitalin (germanicum, y 1 -^ to ^ grain, 0.005 
to 0.01 gram) or digalen (a soluble digitoxin) may be given hypoder- 
mically; or in suitable cases digalen or digitalone may be given intra- 
venously. Digitalin or digalen also may be given by the mouth when 
a prolonged mild effect is desired; but one must remember that most 
of the commercial alkaloids or so-called active principles are inert. 

Digitalis, however, must be employed with circumspection; it is not 
indicated in any case of cardiac disease without evidence of myocar- 
dial insufficiency; nor in cases of rapid, irregular, or overacting heart 



476 DISEASES OF THE ENDOCARDIUM 

unattended with the aforementioned signs of failing myocardium ; nor in 
cases of aortic insufficiency manifested only by dyspnoea, precordial pain, 
anginoid attacks, etc. ; nor, as a rule, in high arterial tension, and angina 
pectoris, except perhaps in some cases in elderly subjects with an asso- 
ciated valvular lesion and failing compensation, in whom it often is of 
much service, and in whom it may be combined with vasodilators. 

As a rule, the drug should be discontinued as soon as the desired 
results have been obtained; it may be resorted to again should the 
indication arise. In cases in which its use has been continued for some 
time, toxic symptoms may develop; but there is little evidence of the 
sudden development of the much-feared so-called cumulative action. 
Nausea and vomiting are the earliest symptoms; these may be followed 
by slowing and weakening of the pulse, lessening in the amount of urine, 
and fall in the blood pressure. More marked evidences of intoxication 
consist of the pulsus alternans, the pulsus bigeminus, and the develop- 
ment of a type of heart block (toxic depression of conductivity and 
contractility). 

Of the substitutes for digitalis, strophanthus (or strophanthin) is the 
best, but it is much less efficient; it is said to cause less vasoconstriction 
than digitalis, and may be used when a mild effect is desired, or after 
the use of digitalis for some time, or in children or elderly subjects. 
Excellent results sometimes attend the intravenous injection of strophan- 
thin (y^-Q- gram, 0.0005 grain). Convallaria, caffeine, adonis venalis, 
sparteine, cactus grandiflorus, squill, etc., occasionally are useful substi- 
tutes, but they are much less efficient than digitalis, and their preparations 
are often inert. Strychnine, iron, arsenic, and alcohol are often very useful 
adjuvants to digitalis, and may be used as the patient convalesces. 

Attacks of acute heart failure, which sometimes are the initial mani- 
festations of final decompensation, but which also frequently develop 
during the persistence of more or less well-marked failure of compensa- 
tion, often demand immediate and active treatment. Frequently the 
attacks are due to obvious causes (dietetic indiscretions, constipation, 
exertion, excitement, etc.) — which should be avoided. When developed 
the attacks should be met with diffusible stimulants and carminatives, 
such as aromatic spirit of ammonia, compound spirit of ether, brandy, 
whiskey, strong coffee, etc., by the mouth; or whiskey, caffeine, cam- 
phor in oil, strychnine, digitalin, strophanthin, adrenalin chloride, etc., 
hypodermically. In many cases the most effective treatment consists 
of prompt venesection and the abstraction of a pint or more of blood. 

The obtrusive symptoms of decompensation are usually relieved by 
improvement of the condition of the heart, but sometimes they require 
special or additional treatment. Dyspnoea not improved by the meas- 
ures already mentioned is commonly due, in part at least, to some asso- 
ciated condition, especially hydrothorax, chronic bronchitis, flatulency, 
dyspepsia, ascites, etc. Hydrothorax (usually right sided) is very com- 
mon and is often overlooked. It should always be sought, and when 
found, paracentesis should be immediately resorted to. This is an 



CHRONIC VALVULAR DISEASE OF THE HEART 477 

exceedingly important therapeutic measure, and is usually promptly 
followed by great relief and improvement in the condition (removal 
of one cause of embarrassed heart action). The dyspnoea due to flatu- 
lent dyspepsia may be controlled by regulation of the diet and the use 
of carminatives, such as brandy, aromatic spirit of ammonia, spirit of lav- 
ender, resorcin, charcoal, sodium bicarbonate, and bismuth. Nocturnal 
dyspnoea, especially the awakening with a start and subsequent dyspnoea, 
should be controlled with morphine hypodermically. Small doses (y-g to 
T X 2 grain, 0.004 to 0.005 gram) often suffice; such is the relief that in 
suitable cases the drug should not be withheld, but its use should not 
be long continued. Nitroglycerin is sometimes of service in cases with 
high arterial tension. Distressing palpitation is usually associated 
with dyspnoea, is due to similar causes, and is to be similarly treated. 
In addition, hot moist applications or an ice bag to the precordium are 
often grateful. The palpitation of excessive muscular hypertrophy is 
often best relieved with tincture of aconite (1 to 2 minims, 0.06 to 0.12 
c.c, thrice daily). Anginoid pains are often provoked, as are attacks of 
palpitation and dyspnoea, and should be similarly met. The anginoid 
pains of aortic lesions are often much benefited by nitroglycerin and 
potassium iodide. Nausea and vomiting require limitation of food, free 
purgation (calomel and salines), and bismuth, cerium oxalate, dilute 
hydrocyanic acid, carbolic acid, creosote, etc., and the non-use of digi- 
talis by the mouth. Restlessness and insomnia are often distressing and 
weakening to the patient. The bromides, valerian, nervines, whiskey or 
brandy in hot water, and hypnotics, such as chloralamid, sulphonal, 
veronal, paraldehyde, etc., are often more or less efficacious; but in 
many cases nothing is comparable to morphine (or codeine or heroin) — 
which in aggravated cases should not be withheld, although it must be 
used with circumspection and not too long continued. Persistence of 
oliguria after several days treatment with digitalis calls for alkaline and 
other diuretics (caffeine, sparteine, theobromine, etc.). An active pur- 
gation (calomel, jalap powder, etc.) is often followed by active diuresis; 
in other cases the so-called Addison's, Guy's, or Niemeyer's pill renders 
excellent service : 

I^ — Powdered digitalis, 

Powdered squill, of each 20 grains 1 3 

Blue mass (or calomel) • 10 grains 05 

Mix and make 20 pills. 

S. — One pill four times daily. 

The ascites and anarasca that do not yield to several days of digitalis 
therapy should be relieved by tapping the abdomen and the use of 
Southey's tubes or aseptic puncture of the legs. Immediate benefit 
often follows, and, as after tapping a hydrothorax, the heart, relieved of 
much embarrassment, is likely to regain its tone. 



478 DISEASES OF THE PERICARDIUM 

DISEASES OF THE PERICARDIUM. 

PERICARDITIS. 

Pericarditis may be variously classified : It may be apparently primary 
(rarely) or secondary (usually); acute or chronic in onset and course; 
circumscribed or diffuse; fibrinous, serofibrinous, purulent, or hemor- 
rhagic as regards the character of the exudate; and tuberculous, strep- 
tococcic, staphylococcic, pneumococcic, etc., as regards the specific 
etiological factor. Inasmuch as an etiological classification is scarcely 
feasible at the bedside, the following clinical classification will be found 
serviceable: Acute and chronic pericarditis; of the acute, the following 
forms: fibrinous, serofibrinous, purulent, and hemorrhagic; and of the 
chronic forms: serous and adhesive. 



FIBRINOUS PERICARDITIS. 

(Dry, Plastic, or Acute Adhesive Pericarditis.) 

Etiology. — Fibrinous pericarditis occurs most commonly in early 
adult life (the eighteenth to the thirty-fifth year), but it may be observed 
also in childhood and in advanced life. It is rare as a primary, common 
as a secondary disorder, and it results always from infection. It is found 
most frequently associated with acute rheumatic fever, but occurs in 
tuberculous, pneumococcic, pyococcic, gonococcic, and influenzal, as well 
as in other infections. It occurs also in chorea, chronic alcoholism, gout, 
diabetes, scurvy, purpura, anemic and cachetic conditions, acute and 
chronic nephritis (frequently as a terminal infection), etc. It is often 
associated with myocarditis and endocarditis, the disease in reality 
being a pancarditis; and it frequently results from extension of disease 
of adjacent structures, such as the mediastinal lmyph nodes (whence 
the frequency of tuberculous pericarditis), the pleurae, the lungs, the 
oesophagus, the vertebrae, the peritoneum, etc. It rarely follows local 
traumatism. 

Pathology. — The lesions may be circumscribed or diffuse. The 
inflamed area becomes hyperemic, swollen, lustreless, and finally 
granular in appearance; and a more or less abundant, thick or thin, 
usually slightly adherent, fibrinous exudation is poured out. In most 
cases, in reality the exudation is serofibrinous, that is, there is always 
some fluid exudation, but this may be minimal (dry pericarditis); the 
fibrinous exudation varies considerably in amount, from a thin semitrans- 
lucent layer to a thick encasement that may completely envelop the heart. 
In cases of moderate fibrinous exudation the motion of the heart gradu- 
ally produces a honeycomb-like, or a bread-and-butter, appearance (cor 



FIBRINOUS PERICARDITIS 479 

villosum). The exudation causes agglutination of the opposed peri- 
cardial surfaces, and, ultimately undergoing organization, may lead to 
the formation of permanent adhesions and pericardial thickening. The 
inflammatory lesions may extend a variable distance into the myo- 
cardium. 

Symptoms. — As a rule, the disease is entirely latent, and is discovered 
during life only when searched for. There may be a little precordial 
pain or distress; and some fever may be present, but this is usually 
an antecedent condition due to the primary disorder; it may be aug- 
mented by the pericarditis. The disease is to be recognized only by 
the detection of the pathognomonic friction sound. This is a peculiar 
rubbing, grating, or creaking, to-and-fro sound, corresponding in gen- 
eral to the systole and diastole of the heart, but not occurring abso- 
lutely synchronously with the cardiac sounds — lagging behind them, 
as it were; this is due to the fact that the greatest systolic excursion of the 
surface of the heart and therefore of its pericardium does not occur 
during the closure-time, but during the expulsion-time of the systole, 
especially at the termination of this period (Geigel). In some cases the 
sounds are systolic or diastolic only; rarely they exhibit a triple rhythm. 
These frictions, as a rule, are best heard over the normal area of super- 
ficial cardiac dulness (where the heart is closest to the chest wall) or 
toward the base, near the root of the aorta; they are often sharply local- 
ized to a small area, which, as a rule, is not a " valve area," and they are 
not transmitted as are endocardial murmurs; they give the impression 
of being superficial, close to the surface; they vary in intensity and 
are sometimes temporarily absent; and they may be intensified by 
the pressure of a stethoscope, a full inspiration, the patient's leaning 
forward, etc. 

Diagnosis. — The diagnosis rests solely upon the detection of the 
characteristic pericardial friction. Pleuropericardial frictions may be 
differentiated by their common situation at the left edge of or beyond 
the limits of the cardiac dulness; by their being much influenced by 
the phases of respiration; that is, although perhaps systolic and dias- 
tolic in time, they are often intensified during expiration and lessened or 
abolished at the height of full inspiration. 

Prognosis. — In many cases the prognosis is that of the primary dis- 
ease, the pericardial lesions being more or less inconsequential. Slight 
lesions may subside, and leave perhaps only a localized area of thick- 
ening of the epicardium (so-called milk-spots); usually, however, more 
or less obliteration of the pericardial sac ensues. If the lesions do not 
subside, they progress to serofibrinous pericarditis. 

Treatment. — The treatment is identical with that of the early stage 
of serofibrinous pericarditis. 



4S0 DISEASES OF THE PERICARDIUM 

SEROFIBRINOUS PERICARDITIS. 

(Pericarditis with Effusion.) 

Etiology. — There is no sharp line of demarcation between fibrinous 
and serofibrinous pericarditis; in many cases they represent different 
stages of the one process — alike etiologically (bacteriologically) and 
pathologically. The cases with much serous effusion, however, are 
most common in young male adults, and are usually associated with 
rheumatism, tuberculosis, or mild pyococcic infections; severe pyo- 
coccic infections usually lead to suppurative pericarditis. 

Pathology.— In the early stage the lesions are identical with those of 
fibrinous pericarditis. Soon, or in some cases from the beginning, 
a more, or less abundant fluid exudate is poured out — thin, serous, 
yellowish, alkaline, albuminous (3 to 7 per cent.), usually at least 
slightly turbid, and often containing fibrinous flacculi; occasionally the 
fluid may have a greenish tint or it may be purulent or hemorrhagic 
(suppurative or hemorrhagic pericarditis). The fluid varies in amount, 
as a rule, from 100 to 2000 c.c. In favorable cases the inflammatory 
lesions subside, and are followed by whitish patches, so-called "milk 
spots" (evidences of past circumscribed pericarditis), or total oblitera- 
tion of the sac (evidences of past diffuse pericarditis). In some 
cases the acute lesions become subacute and finally chronic, and lead 
to partial obliteration of the pericardial sac associated with a small 
amount of fluid. In these cases exacerbations may occur. In most, 
especially severe cases, the heart shows more or less marked interstitial 
myocarditis, and parenchymatous and perhaps fatty degeneration of the 
muscular fibers. 

Symptoms. — Serofibrinous pericarditis, occurring in the course of many 
of the infectious diseases, frequently runs its course entirely unsuspected; 
in other cases extensive collections of fluid occasion but little distress, and 
are only accidentally discovered by physical examination (latent cases). 
In some severe cases certain well-marked though non-characteristic 
symptoms occur. 

The general symptoms are those of the primary disease, and moderate, 
irregular fever — 102° to 103° F. The local symptoms consist of pain, 
which is usually moderately distressing, but which may be severe or 
may be absent; and dyspnoea, in some cases progressing with the out- 
pouring of the exudation to orthopnoea, and the other results of pressure 
(such as, paroxysmal cough, aphonia, pulsus parodoxus, etc.). Further- 
more, the accumulating fluid, increasing the intrapericardial tension, 
interferes with the diastole of the heart, and the inflammatory alterations 
(of the myocardium as well as of the pericardium) interfere with the 
systole of the heart; these lead to pallor, cerebral anemia, and headache, 
and later cyanosis and aggravation of the dyspnoea (in part due also to 
compression of the lungs, especially the left), and a small, weak, and 



SEROFIBRINOUS PERICARDITIS 481 

irregular pulse. In severe cases toxic symptoms are marked — vomiting, 
sweats, mental hebetude, coma, delirium, etc. 

Physical Signs. — Physical signs are necessary to the diagnosis. In 
the first stage there are the usual signs of cardiac excitement, such as 
excitation and frequency of the heart action, accentuated sounds, etc.; 
possibly a palpable friction fremitus; sometimes a little increase in the 
transverse cardiac dulness (from dilatation); and the pathognomonic 
friction sounds on auscultation. As the fluid accumulates, the apex 
becomes weak, and ultimately, as a rule, disappears. The maximum 
palpable impulse is often in the fourth or the third intercostal space; 
this is often erroneously interpreted as the apex beat, but, as a 
matter of fact, in most cases the position of the heart is not much 
changed; in large effusions it often descends with the descent of the 
diaphragm, being somewhat influenced also by the size of the heart 
(whether compressed or dilated). Often the apex beat can be palpated 
in or near its normal situation by having the patient lean forward. 
Especially in young subjects, as the fluid increases the pericardium 
may bulge and the interspaces become widened; in purulent cases 
there may be some oedema of the overlying skin and subcutaneous 
tissues. 

The area of cardiac dulness becomes increased in all directions (lat- 
eral displacement of the pulmonary margins). Of especial importance 
is the fact that it is no longer possible to distinguish an absolute (or 
superficial) and a relative (or deep) cardiac dulness; the dulness is 
absolute throughout, and the resistance is greatly increased. The dul- 
ness varies much in shape in different cases : it is often described as 
irregularly triangular with a blunt apex above on a level with the second 
left rib or interspace, and a broad base below, extending from near the 
right mammillary line to beyond the left (depending upon the amount 
of fluid). In some cases the area of dulness is distinctly pear-shaped 
(or pyriform); in others the shape is that of a truncated cylinder, or 
trapezoidal, or is quite irregular. The shape is generally devoid of much 
diagnostic significance. Important signs in connection with the dulness 
are: disproportionate extension to the right and upward; dulness in the 
right fifth intercostal space extending one to two inches to the right of 
the sternum (Rotch's sign) ; an obtuse (rather than a right-angled or an 
acute) cardiohepatic (E ostein's) angle; extension of the dulness to the 
left beyond the still perceptible apex (or heart) beat; change in the 
shape and extent of the dulness with change in the posture of the patient 
— a larger area of dulness when the patient leans forward than when he 
is erect or recumbent, and disproportionate displacement laterally toward 
the lower side when the patient is on his side; dulness near the angle of 
the left scapula, associated with bronchial or bronchovesicular breathing, 
bronchophony, and increased vocal fremitis (Bamberger's sign), which 
disappear or lessen when the patient leans forward (anterior prone or 
knee-chest posture) and breathes deeply. Similar phenomena may be 
encountered in the left axilla and in the right mammary region. These 
31 



482 DISEASES OF THE PERICARDIUM 

signs are attributable to compression of the lung, or, as suggested by 
Ewart, to an altered position of the liver. The diaphragm and the left 
lobe of the liver are displaced downward, and may give rise to a visible 
and palpable bulging of the epigastrium. Compression of the left lung 
anteriorly may cause, in the infraclavicular region, a vesiculotympanitic 
note (skodaic resonance) or dulness. 

In most cases, as fluid accumulates, the friction sounds lessen and 
may entirely disappear (especially in large effusions); often, however, 
they merely become more restricted in area, being still audible at or 
toward the base of the heart. In the absence of valvular disease the 
heart sounds are intact, although in the early stages they are more or 
less obscured by the frictions, and they become progressively less loud 
(muffled) as the fluid accumulates, until they may become quite faint 
and distant. As the fluid becomes absorbed, there is a gradual disap- 
pearance of the abnormal and a gradual return of the normal physical 
signs. 

Diagnosis. — The condition is frequently overlooked, because of its 
practically symptomless course; many cases are latent, and others are 
fleeting, developing and disappearing with great rapidity, especially 
in the terminal stages of divers disorders. The diagnosis must be based 
wholly upon the physical signs. Less than 100 c.c. of fluid is scarcely 
susceptible of recognition. The nature of the fluid cannot be determined 
by the physical signs, but in rheumatic and tuberculous cases it is usually 
serofibrinous, but it may be purulent in tuberculosis; it is usually 
purulent in pyococcic infections; and hemorrhagic in some tuberculous 
cases, and in purpura, scurvy, leukemia, and anemic and cachectic 
conditions. It is often difficult to distinguish between pericardial 
effusion and dilated heart, but in dilated heart there is usually a visible 
wavy pulsation over much of the precordium; the superficial and the 
deep cardiac dulness may be differentiated; the dulness is more globular 
in shape, and rarely reaches as high along the right edge of the sternum, 
or as far out into the fifth intercostal space, and if it does there is usually 
a visible and a palpable impulse; Ebstein's cardiohepatic angle remains 
acute, or at most is a right angle; and the heart sounds are usually clear, 
sharp, and valvular, and a gallop rhythm may be audible. Difficulty 
is sometimes experienced in differentiating pleural effusion, but careful 
physical exploration should enable one to make the proper diagnosis. 

Prognosis. — The prognosis depends upon the nature of the causative 
factors. Most cases due to rheumatism or tuberculosis recover after 
ten days or two weeks with adhesions (chronic pericarditis). In cases of 
severe infection, with severe general symptoms, a large amount of fluid, 
associated valvular disease or chronic nephritis, the prognosis is anxious ; 
such cases often terminate fatally. Some cases become subacute and 
chronic. 

Treatment. — In all cases, even the mildest, the patient must be con- 
fined to bed, and he should be given a light, liquid and semisolid, nutri- 
tious diet. In general the treatment must be based upon the primary 



PURULENT PERICARDITIS 483 

disorder (rheumatism, tuberculosis, nephritis, leukemia, etc.), if this 
can be determined. In many, especially rheumatic cases, prompt sub- 
sidence of the phenomena follows the administration of the salicylates 
(as recommended in rheumatism). The pain and discomfort of the 
early stages not thus relieved may be mitigated by the local application 
of cold (dry or wet), cupping, the use of leeches, or by a hypodermic 
injection of morphine and atropine; or one may use the opium and 
quinine pill recommended for acute pleuritis. A blister is believed by 
some observers to prevent or limit the effusion. When once formed, the 
fluid, as a rule, tends to become absorbed spontaneously. Absorption 
may be hastened by counterirritation (blisters or iodine locally), a light 
dry diet (very little fluid), a salt-poor diet, diuresis (infusion of digitalis 
and potassium acetate and citrate), and catharsis (concentrated saline 
cathartics before breakfast). Signs of embarrassed cardiac action (fre- 
quent heart beat, pulsus paradoxus, low blood pressure, pulmonary 
and general venous engorgement) call for withdrawal of the fluid — by 
paracentesis in serofibrinous effusion, by incision and drainage in 
purulent effusion. For paracentesis the puncture may be made in the 
fifth interspace in or outside the midclavicular line, depending upon the 
distention of the pericardium, in the fifth or fourth intercostal space 
along the left edge of the sternum, or in the costoxyphoid angle (directing 
the trocar upward and backward). Should serious cardiac weakness 
develop at any time, stimulants, such as alcohol, camphor, ether, digi- 
talis, strophanthus, etc., should be resorted to, and withdrawal of the 
fluid should not be delayed. 



PURULENT PERICARDITIS. 

(Suppurative Pericarditis; Empyema of the Pericardium.) 

Etiology. — Suppurative pericarditis is a secondary disorder that some- 
times occurs in the course of various pyococcic infections (pneumonia, 
pleural empyema, general septicopyemia), tuberculosis, etc. It may 
begin as a serofibrinous pericarditis, or it may be suppurative from 
the beginning. 

Pathology. — In cases in which the fluid exudate is rather thin (sero- 
purulent), the changes are quite like those of serofibrinous pericarditis, 
but intensified; the fluid is more opaque and contains more cells, the 
pericardium is thickened and covered with a thick fibrinopurulent 
exudate, and there is a marked polynuclear leukocytic infiltration of the 
pericardium. In the frankly purulent cases the fluid is thicker, dis- 
tinctly purulent. The lesions, as a rule, extend a variable distance 
into the myocardium, which may become the seat of disseminated 
purulent foci; the lesions may even extend to and involve the endo- 
cardium. The exudate rarely becomes in part absorbed, inspissated, 
and calcified. 

Symptoms. — In some cases, the onset and the course of the disease 
for some time are identical with those of serofibrinous pericarditis, of 



484 DISEASES OF THE PERICARDIUM 

which the suppurative process may be an advanced stage. In other 
cases, following antecedent symptoms of the primary disorder, the 
development of the pericarditis may be abrupt, with a chill, high tempera- 
ture, pain, or distress in the precordial region, and general evidences 
of toxemia, notably delirium (peculiar to pericarditis). In many cases 
the purulent character of the exudate is not suspected for some time, 
unless the disease develops in a frank case of septicopyemia. Con- 
tinuance of fever otherwise explained, however, suggests the purulent 
character of the exudate, as do also progressive pallor, weakness, loss 
of flesh, and paroxysms of chills (or chilliness), fever, and sweats, and 
polynuclear leukocytosis. The physical signs are identical with those 
of serofibrinous pericarditis; that is, the physical signs do not disclose 
the character of the exudate. (Edema of the overlying skin and sub- 
cutaneous tissues is quite significant of suppuration. 

Diagnosis. — The diagnosis depends upon the physical signs of fluid 
in the pericardium, oedema of the overlying skin, general and local 
evidences of septicopyemia, and the results of exploratory puncture; 
this should not be neglected nor long postponed in doubtful cases. 

Prognosis. — The prognosis is bad, as a rule, on account of the process 
itself and of the usually pyococcic infections of which it is a part. 

Treatment. — The treatment is essentially surgical — incision and drain- 
age, which should be instituted as soon as the diagnosis is made; and, 
as stated, attempts should be made to recognize the condition as soon 
as possible by resort to exploratory puncture. Otherwise the treatment 
is that of pyococcic infections in general. 



CHRONIC PERICARDITIS. 

Chronic pericarditis occurs in three forms: 

1. White Patches or "Milk Spots." — These are usually found 
on the anterior surface of the visceral pericardium. Usually they are 
evidences of previous localized pericarditis, although they have been 
attributed to a low grade of chronic hyperplasia of the connective tissue, 
the consequence of the mechanical irritation occasioned by the continued 
impact of the heart against the resisting chest wall. Commonly insus- 
ceptible of diagnosis, the condition is of no clinical importance, except 
in that it may be the source of frictions, sometimes interpreted as endo- 
cardial murmurs in apparently healthy persons. 

2. Chronic Pericarditis with Effusion. — The exudate is usually 
serofibrinous, sometimes hemorrhagic in character, and not infrequently 
there are some soft adhesions or partial obliteration of the sac. Tuber- 
cles may be detected by macroscopic and microscopic examination. 
Sometimes an apparently primary disorder, it is usually part and parcel 
of a more or less widespread tuberculosis. The disease is suggested by 
general and gradual failure of health, subacute onset, chronic course, 
"tuberculous habitus," the constitutional symptoms of tuberculosis, 



CHRONIC PERICARDITIS 485 

tuberculosis in the antecedents, tuberculous foci in other parts of the 
body, and the physical signs of pericardial exudation, its persistence, 
and the physical signs of fluid in other serous cavities. In the absence 
of clear evidence of tuberculosis elsewhere in the body, diagnostic help 
may be found in tuberculin injections, and in the injection of the fluid 
exudate into guinea-pigs. The prognosis is unfavorable. The treat- 
ment is that of tuberculosis in general, and of serofibrinous pericarditis. 

3. Adhesive Pericarditis (Obliterative Pericarditis; Adherent 
Pericardium; Concretio Cordis cum Pericardio ; External Pericarditis; 
Pleuropericarditis ; Indurative Mediastinopericarditis) . — Inasmuch 
as chronic obliterative pericarditis, external pericarditis, pleuroperi- 
carditis, and indurative mediastinopericarditis in many cases represent 
but stages of the same disease, and can scarcely be differentiated the 
one from the other, it is the part of wisdom and utility to discuss them 
together. 

Etiology. — Adhesion of the two layers of the pericardium may be 
the consequence of a previous acute pericarditis, but the absence of 
symptoms in some cases leads to the inference that the lesions were 
chronic from the beginning. It is sometimes tuberculous in nature; 
and occurs in rheumatic, syphilitic, and nephritic subjects. 

Pathology. — The two layers of the pericardium are usually intimately 
and completely adherent, and in many cases also much thickened, in 
consequence of hyperplasia of the connective tissue and the organi- 
zation of a fibrous exudate. At times the adhesions being incomplete, 
the space thus left may contain more or less serofibrinous or inspissated 
and caseous material. More or less extensive calcification is not very 
uncommon. Associated with obliteration of the pericardial sac (internal 
pericarditis) there is frequently external pericarditis and indurative 
mediastinitis (adhesion of the pericardium and the heart to the chest 
wall, the pleurae, lungs, and tissues of the mediastinum); in some cases 
also obliteration and extensive thickening of the pleurse; and in other 
cases adhesions to the under surface of the diaphragm (perihepatitis, peri- 
splenitis, and deforming peritonitis — multiple serositis) may be observed. 
If the adhesions are slight or moderate the heart may show little or no 
change for a long time. Usually, however, inasmuch as the adhesions 
are dense and extensive, there is more or less extensive hypertrophy of 
the heart and fibrous myocarditis, which in time are succeeded by dila- 
tation. 

Symptoms. — Clinically three classes of cases may be distinguished: 
(1) Cases in which the pericarditis runs its course entirely devoid of symp- 
toms, and constitutes merely an accidental finding at necropsy; (2) cases 
in which, sooner or later, symptoms of disturbed or impeded cardiac 
action manifest themselves, and in which from the physical signs the 
obliterative pericarditis is more or less susceptible of diagnosis; and 
(3) cases characterized clinically by marked ascites, with little or no 
oedema of the legs, cases in which the diagnosis of cirrhosis of the liver 
is usually made, and which at the necropsy reveal chronic obliterative 



486 DISEASES OF THE PERICARDIUM 

pericarditis and certain morbid changes in other tissues and organs — 
notably pleuritis, peritonitis, perihepatitis, nutmeg liver, red atrophy 
of the liver, cirrhosis of the liver, etc. 

In the majority of instances when chronic adhesive or obliterative 
pericarditis gives rise to symptoms, the symptoms that arise are those 
of failing cardiac compensation — palpitation of the heart, dyspnoea, 
cough, cyanosis, generalized oedema, effusions into the several serous 
cavities of the body, etc. On the contrary, in the cases that simulate cir- 
rhosis of the liver, clinically, the first symptoms are sensations of fulness, 
oppression, and weight in the upper abdomen, or there may be appar- 
ently a sudden onset with acute pain; the abdomen increases in size and 
may attain very large dimensions — due evidently to ascites that may 
necessitate repeated tappings (Rumpf's patient was tapped 301 times). 
With increase in the amount of the ascites the abdominal walls 
become tense and painful, and the other subjective symptoms become 
markedly aggravated. There may be slight and transitory jaundice. 
Later, oedema of the legs may develop. In a few cases oedema of the 
legs comes on early; it may remain but a short time, disappear, and not 
recur until shortly before the death of the patient. In rare cases it 
persists; but it is always inconspicuous when contrasted with the exces- 
sive and constantly recurring ascites, and it scarcely attracts attention. 

Physical Signs. — Physical signs are essential to the diagnosis. Of 
these the most important are: A weak or absent apex beat, especially 
significant in cases in which there is no increase n the area of cardiac 
dulness; systolic retraction of a considerable area about the apex-beat; 
systolic retraction of the base of the left chest posteriorly, in the region 
of the eleventh or twelfth rib (Broadbent's sign), attributable to adhesion 
of the heart, pericardium, and diaphragm, and a systolic tug upon the 
diaphragm which becomes communicated to its point of attachment 
to the chest wall posteriorly; arrest of the normal respiratory movements 
in the epigastric angle; a systolic tug in the epigastrium or in the neigh- 
borhood of the left seventh or eighth costal cartilage; imperfect descent 
of the apex beat during inspiration; inadequate or entire absence of 
shifting of the apex beat, with change in the posture (lateral posture) 
of the patient; absence of change in the limits of cardiac dulness during 
the respiratory phases; absence of increase of the cardiac dulness to the 
right, despite marked engorgement of the veins of the neck; a diastolic 
shock or rebound of the heart and precordium; evidences of dilatation 
or hypertrophy of the heart (which may be marked) in the absence of 
valvular or other disease that might cause it; absence of the character- 
istic changes in the heart in the presence of definite valvular disease — 
that is, absence of the usual hypertrophy of the right ventricle in mitral 
valve disease, and of the left ventricle in aortic valve disease; absence 
of pericardial effusion in the presence of pleural and peritoneal effusions ; 
paradoxic pulse — inspiratory diminution in the force and volume of the 
arterial pulse; diastolic collapse of the veins of the neck (Friedreich's 
sign); inspiratory swelling of the veins of the neck (Kussmaul's sign); 



HEMOPERICARDIUM 487 

a presystolic murmur (Fisher's sign) in the absence of other evidences 
of mitral stenosis or of aortic insufficiency (Flint murmur); and, as 
suggested by Musser, the non-occurrence in young subjects with val- 
vular disease and cardiac insufficiency of the characteristic improvement 
following the administration of digitalis. None of these signs is pathog- 
nomonic of adherent pericardium; all will not be present in every case, 
but in many cases a sufficient number will be present to warrant the 
diagnosis. 

Prognosis. — From the nature of the disorder, restoration to the normal 
is impossible. The outlook depends upon the establishment and main- 
tenance of an efficient hypertrophy of the heart. 

Treatment. — The treatment is that of myocardial insufficiency and 
cardiac decompensation in general. Brauer has suggested loosening 
the adhesions surgically (cardiolysis), an operation perhaps permissible 
in young subjects and in others in whom the myocardium is in good 
condition. 

HYDROPERICARDIUM. 

(Dropsy of the Pericardium; Pericardial Transudate.) 

Hydropericardium, the transudation of non-inflammatory fluid into the 
pericardial sac, is a secondary process that occurs in conditions which 
lead to oedema generally, such as chronic heart disease with decompen- 
sation, as well as chronic disease of the lungs that induce myocardial 
disorders; it occurs also in the advanced stages of chronic nephritis, 
and in anemia and cachectic states generally (carcinoma, sarcoma, 
pernicious anemia, leukemia, scurvy, etc.), in consequence of hydremia 
and perhaps diseases of the capillary vessel, and toxemia. The symp- 
toms are scarcely suggestive, and, as a rule, are overshadowed by those 
of the primary disorder; dyspnoea, cyanosis, and other evidences of 
cardiac embarrassment, are usually marked. Hydropericardium is 
suggested by the primary causative factors, the physical signs of fluid 
in the pericardium, the absence of friction sounds and of fever, and the 
presence of fluid in the other serous sacs. The prognosis is bad. The 
treatment is that of the primary cardiac, renal, or other disorder, to which, 
should the symptoms be urgent, paracentesis of the pericardium should 
be added. 

HEMOPERICARDIUM. 

(Blood in the Pericardium.) 

In many cases of serofibrinous pericarditis the fluid exudate contains 
a variable number of erythrocytes, which, however, usually pass un- 
noticed, unless the fluid is examined microscopicly. Sometimes the 
erythrocytes are present in such numbers as to give a more or less well- 
marked hemorrhagic tint to the fluid. This occurs, especially in certain 
cases of tuberculosis, attended by the eruption of miliary tubercles 



488 DISEASES OF THE PERICARDIUM 

in the pericardium (rupture of new-formed capillaries); in primary and 
secondary tumors of the pericardium; in asthenic and cachectic states, 
such as chronic nephritis, purpura, scurvy, leukemia, etc. More obvious 
blood in the pericardium may result from perforating ulcers of adjacent 
organs (oesophagus, etc.), and it may be due to rupture of the heart or 
of an aneurysm of the ascending aorta. In the first-mentioned cases 
the symptoms and physical signs are those of serofibrinous pericarditis 
with exudation; in the last mentioned, those of sudden heart failure, 
usually soon succeeded by death. 



PNEUMOPERICARDIUM; PYOPNEUMOPERICARDIUM. 

(Air and Gas in the Pericardium.) 

Pneumopericardium or pyopneumopericardium is a rare condition 
that may result from trauma (or wounds); from perforation from an 
adjacent air-containing organ, such as the lung, bronchus, oesophagus, 
stomach, or intestines; or from infection by Bacillus aerogenes cap- 
sulatus. Infection by Bacillus aerogenes capsulatus usually occurs 
shortly before death, and the lesions are those of a pyopneumoperi- 
carditis without clear cause. Most cases result from perforation of an 
adjacent air-containing viscus, such as rupture into the pericardium 
of a pulmonary cavity, abscess, or gangrenous focus, or pyopneumo- 
thorax, or of an esophageal carcinoma, or of a gastric ulcer or gastric 
carcinoma. In addition to the gas the pericardium may also contain a 
fluid transudate, which in the great majority of cases is purulent. In 
rare and slightly advanced cases it may be only serofibrinous. 

Symptoms.— The symptoms are those of pericarditis. The diagnosis 
rests entirely upon the result of the physical examination. In the recum- 
bent posture the precordium is tympanitic, partly or entirely, depending 
upon whether there is little or much fluid. In most cases the note changes 
when the patient assumes the upright posture — the tympany low down 
giving way to dulness occasioned by the fluid exudate, or the heart 
itself. The dulness is still more noticeable in the knee-chest posture. 
The characteristic physical sign is a peculiar metallic splashing sound, 
caused by the heart churning up the fluid and gas; it is often very loud, 
and may be heard at a distance from the patient. A somewhat similar 
quality, however, may be given to the heart sounds by a distended sto- 
mach, a stomach drawn up, or pushed up, or by a pneumothorax. 

The prognosis is hopeless except in a few traumatic cases, in which 
appropriate surgical treatment, incision, and drainage are instituted early. 



CHYLOPERICARDIUM. 

Chylopericardium has been observed in filariasis. 



ARTERIOSCLEROSIS 489 

DISEASES OF THE ARTERIES. 

ACUTE AORTITIS. 

Acute aortitis is a rare and ill-defined disorder that is said to occur 
in certain infections, especially those due to the pyococci (so-called 
malignant endocarditis, puerperal infection, etc.), but also in typhoid 
fever, pneumonia, influenza, tuberculosis, etc. The lesions are analogous 
to those of acute endocarditis. Acute lesions may be superadded to 
chronic, arteriosclerotic, or atheromatous changes. The peripheral 
arteries also may be involved, and it is not unlikely that minor acute 
lesions, occurring perhaps not uncommonly in acute infections, are the 
starting point of the more chronic lesions of later life. There are no 
unequivocal symptoms, although substernal distress and tenderness, 
palpitation of the heart, dyspnoea, anginoid pain, and the physical 
signs of dilatation of the arch of the aorta (without concomitant signs 
of aneurysm) are said to be significant of acute aortitis. There may be 
some fever, and signs of arterial embolism. The diagjiosis must be always 
in doubt. The treatment is that of acute endocarditis. 



ARTERIOSCLEROSIS. 

(Arterio-capillary Fibrosis; Atheroma; Angiosclerosis; Atherosclerosis; Chronic 
Deforming Endarteritis.) 

Arteriosclerosis is a term used to denote the series of changes, largely 
degenerative in nature, to which the arteries are subject, and of which 
the conspicuous feature is fibrosis. 

Etiology. — Arteriosclerosis is a normal manifestation of advancing 
age, being found in varying degrees after the fortieth year. It is much 
more common, and present in higher grade, in men than in women; 
the onset in women is commonly later in life than in men. The chief 
causes of presenile arteriosclerosis are syphilis, chronic alcoholism, 
chronic nephritis, plumbism, gout, diabetes, excessive muscular work, 
excessive eating and drinking, excessive and prolonged mental work and 
worry, etc. This presenile arteriosclerosis also is much more common 
in men than in women, largely on account of the etiological factors. 
The disease is rare in children, and when occurring in them seems to be 
related, if not to the ordinary causes, to infections, such as typhoid 
fever, scarlatina, influenza, etc. This may be the starting point of an 
arteriosclerosis that becomes more or less obtrusive in later life. 

Pathology. — Adami points out that in the aorta and its main branches 
three forms of arteriosclerosis may be distinguished: (1) Nodose arterio- 
sclerosis, which shows itself in the slightest cases, as a thickening and 
sclerosis, more particularly at or around the origins of the branches 



490 DISEASES OF THE ARTERIES 

of the aorta, as yellowish-white thickenings notably affecting the origins 
of the intercostal arteries. Later these grow in size and some of them 
coalesce, forming in the opened aorta projecting flattened nodes; these 
may be scattered somewhat irregularly through the aorta, tending to be 
more abundant and more advanced in the abdominal region. This 
is the form especially that passes into atheromatous degeneration and 
softening, the breaking down of the affected region into a granular 
debris — so-called atheromatous abscess; calcification may occur and 
lead to the formation of a so-called atheromatous plaque. (2) Senile 
arteriosclerosis, which is characterized by the presence of hardened 
and at times pipe-stem radial and other arteries; but in the aorta there 
may be a complete absence of nodose thickening of the intima. In its 
place there is a diffuse dilatation of the aorta, affecting more partic- 
ularly the thoracic portion; the aortic walls are thinned, instead of 
thickened, and the increased volume of the aorta tends to show itself 
not only in breadth, but also in length, the vessel being somewhat 
tortuous; the arch takes a wider sweep, the abdominal section is curved. 
In the common iliac and the carotid arteries there are slight depressions, 
tending to have their long axes situated transversely — the reverse of the 
sclerotic nodosities, a giving way taking the place of thickening of the 
wall. Although there may be a diffuse thickening of the intima of 
moderate grade in these cases, it is not the cause of the hardening of the 
arteries, this being due to calcification of the media (Klotz), which is 
likely to be preceded by marked hypertrophy of the middle coat. This 
Adami regards as the uncomplicated type of senile arteriosclerosis 
(Monckeberg's type), but it is relatively uncommon; the commonest 
condition in elderly people being a combination of the two types men- 
tioned. (3) Syphilitic arteriosclerosis, which has its seat of election 
in the ascending aorta and the arch, where the nodes are likely to lie 
in groups. These in their earlier stage are large, succulent, and semi- 
translucent or hyaline in appearance ; they have little tendency to athero- 
matous or calcareous change, but exhibit a later scarring or central 
depression with some puckering. Adami further states that the primary 
disturbance in these cases is a subacute mesaortitis, with small-celled 
infiltration around branches of the vasavasorum and absorption of the 
elements proper of the media. Coincidently there is overgrowth of the 
intimal tissue, and when as a result the deeper portions of the over- 
growth exhibit necrotic change and degeneration, the underlying inflam- 
matory granulation tissue advances new capillaries into the necrotic 
area. The result is an absorption of the degenerated material, replace- 
ment by cicatricial tissue, shrinkage, and scarring. There is a lack of 
this vascularization and replacement in the ordinary nodose arterio- 
sclerosis. Adami speaks of the smaller arteries as — the muscular arteries 
and the arterioles : the muscular arteries exhibit changes similar to those 
mentioned in the three types of sclerosis, but there is less atheromatous 
and degenerative change; the calcification that does occur in the middle- 
sized arteries involves the media more than the intima; and there is 



ARTERIOSCLEROSIS 491 

more or less diffuse thickening of the intima and overgrowth of the 
intima, suggesting a change to compensate for thinning of the media; 
the arterioles exhibit in general similar changes, but in one series of cases 
hypertrophy of the muscular coat is the dominating change, in another 
series fibrosis is the most evident alteration — fibrosis of the intima, 
fibrosis replacing largely the muscular tissue of the media, and fibrosis 
and pronounced overdevelopment of the adventitia. 

Adami describes the following as the effects of syphilis on the aorta, 
and states that the lesions of the other forms of arteriosclerosis are 
quite similar: The primary disturbance is a granulomatous inflam- 
matory degeneration of the media, which leads to a local giving way 
of the media (fatty degeneration, necrosis, and calcareous infiltration 
of the muscular fibers, and loss of elasticity of the elastica). If this 
giving way be moderate, it results in a strain hypertrophy of the intima 
and the adventitia, with the development of nodose intimal sclerosis; 
if it be extreme, overstrain, atrophy of the intima, and aneurysmal forma- 
tion ensue. The intimal nodosities are not of inflammatory type and are 
non-vascular, although with the progressive laying down of layer upon 
layer of connective tissue on the more internal aspect of the intima the 
earlier and deeper placed layers of new tissue gain less and less nourish- 
ment, and are likely to exhibit fatty degeneration and necrosis. These 
products of necrosis exert a chemotactic influence upon the nearby 
vessels of the medial granulation tissue, with, as a result, a secondary 
and later entrance of new vessels into the early and deeply placed 
atheromatous area, absorption of the necrotic products, replacement 
by granulation tissue, contraction of the granulation tissue, and depres- 
sion and scarring of the sclerotic nodules so characteristic of syphilitic 
sclerosis. Strain and overstrain are believed to be of the greatest 
importance. As regards the significance of heightened blood pressure 
(hyperpiesis, Allbutt), Adami reaches the conclusion that like results 
may ensue when, on the one hand, the artery has undergone weakening 
and the blood pressure is normal, and when, on the other hand, the 
artery has no preliminary degeneration of its media and the blood 
pressure is above the normal. The increased blood pressure may be 
variously provoked. By some observers it has been attributed to hyper- 
activity of the adrenals, perhaps induced by divers toxic causes. 

Symptoms. — The symptoms, like the lesions, as a rule, are insidious 
in onset and slow in progression, although rarely they seem to develop 
with considerable celerity. Even considerable degrees of arteriosclerosis, 
however, may be present for years without occasioning notable symp- 
toms, and symptoms when they do occur are most diverse in nature, 
due to the fact that although the arteriosclerotic process may be wide- 
spread, the lesions are often unequally pronounced in different parts 
of the body. 

In the early stages there is lessened elasticity and contractility of the 
vessels and consequent imperfect and irregular distribution of the blood — 
which may be a more or less permanent condition or only induced by 



492 DISEASES OF THE ARTERIES 

exertion, fatigue, etc., and the ensuing symptoms are correspondingly 
variable. In general they are those of lessened vigor and vitality, of 
fatigue, neurasthenia, etc. The patient readily becomes tired, even 
more or less exhausted ; he is nervous and irritable, unable to concentrate 
his attention as formally, and suffers from headache, vertigo, insomnia, 
or somnolence; exertion may provoke various painful sensations, such 
as headache, paresthesias, neuralgiform pains, or muscular cramps; 
the functional activity of the special senses (especially hearing and 
sight) becomes impaired; and various other symptoms develop, depend- 
ing upon the special prominence of the lesions in the different organs. 

Those referable to the cardiovascular system naturally are usually in 
the ascendency. The heart passes through all the stages from efficient 
hypertrophy to final dilatation and decompensation. More or less 
dyspnoea and palpitation of the heart are usually present on exertion; 
epistaxis and other hemorrhages are not uncommon; later, oedema and 
other signs of cardiac failure supervene. In general appearance the 
patient may be ruddy, full-blooded, or he may be pale and anemic 
looking — which is due to imperfect distribution of the blood, and not 
to poor blood, at least in the beginning. In the early stages major 
diagnostic importance attaches to visible and palpable evidence of 
thickening and tortuosity of the superficial arteries, to increased blood 
pressure (160 to 180 mm. Hg. or more), to the physical signs of hyper- 
trophy of the left ventricle, a dull, prolonged, somewhat muffled first 
sound at the apex of the heart (augmented muscular element), an 
accentuated aortic second sound, and a sloping ascent, broad apex, 
and slow decline of the pulse wave, especially apparent in tracings. 
Ultimately the common signs of dilatation ensue; indeed, these may be 
the symptoms presented by the patient when he first comes under 
observation. Involvement of the coronary arteries may lead to angina 
pectoris, the fibroid heart, aneurysm of the heart, thrombosis with 
sudden death, etc. 

Renal symptoms are often quite conspicuous — those of chronic dif- 
fuse indurative (interstitial) nephritis; indeed, in most cases, the disor- 
der is correctly described as cardiovascular-renal disease. Symptoms 
referable to the nervous system are often prominent; of these, the 
most important are headache, vertigo, tinnitus aurium, incapacity for 
work, and irritability; transitory attacks of hemiplegia, monoplegia, 
or aphasia (sometimes attributed to arterial spasm and consequent 
temporary anemia); cerebral hemorrhage (often the immediate cause 
of the fatal issue). 

Gastro-intestinal symptoms — that is, so-called indigestion, but also 
some cases of gastric ulcer, are sometimes attributed to special in- 
volvement of the supplying vessels. Special interest attaches to 
attacks of severe abdominal pain (abdominal angina) that come on 
several hours after eating, and may be associated with other anginoid 
phenomena, such as angina pectoris; they are attributed to spasm of 
the gastric and mesenteric vessels. Severe painful cramps in the legs 



ANGINA PECTORIS 493 

induced by walking are not infrequent (intermittent claudication or 
lameness); the disorder is due to temporary anemia of the affected 
parts, and is characterized by the absence of symptoms when at rest, 
by their provocation by walking, by their cessation upon resting, and 
often by the absence of a palpable pulsation in the pedal arteries. 

Obstruction to arteries elsewhere may give rise also to local pain, and 
if the obstruction become complete gangrene may follow. 

Diagnosis. — The diagnosis may be suggested by the known habits 
of the patient, his general appearance (full-blooded or anemic looking), 
and gradual impairment of vigor and vitality; confirmation of the 
diagnosis is found in the obvious condition of the peripheral arteries, 
the hypertrophy of the left ventricle, an accentuated aortic second 
sound, and the pulse. In most cases also the blood pressure will be 
found high, but in many quite advanced cases, the blood pressure is 
low, perhaps normal or less. All early diagnoses may sometimes be 
made by ophthalmoscopic examination of the retinal vessels. 

Prognosis. — The outlook in general is unfavorable, but it should not 
be exaggerated, since the disorder is one evidence of advancing age, 
Occurring in young subjects, however, arteriosclerosis usually shortens 
life, and is dangerous on account of the possibility of apoplexy, uremic 
manifestations, heart failure, etc. In many cases the progress of the 
disease may be stayed by appropriate treatment. 

Treatment. — The disorder can be more readily prevented than cured. 
All the known causative factors should be avoided, especially excessive 
eating and drinking, alcohol, tobacco, tea and coffee, excessive mental 
and bodily work, etc., and the patient should be instructed to lead a 
quiet life free from unnecessary cares and excesses of all kinds. Dis- 
eases known to lead to arteriosclerosis should be efficiently treated, 
especially syphilis, gout, diabetes, lead poisoning, chronic nephritis, etc. 
In many even non-syphilitic cases the iodides seem to do good, and may 
be given (30 grains, 2 grams, daily) for a month at a time and then dis- 
continued for a month. Excessive blood pressure should be reduced by 
nitroglycerin (not longer than three or four weeks at a time), sodium 
nitrite, erythrol tetra-nitrate, free catharsis, a low diet, and rest; but 
one must remember that some of the increased pressure is a conserva- 
tive process, and an attempt to reduce the pressure to normal should 
not be made. Much benefit often attends a course of treatment at one 
of the well-known spas, or a course of massage, passive exercise, and 
warm baths. When the heart begins to fail, the treatment is that of 
the fibroid heart. 

ANGINA PECTORIS. 

(Stenocardia; Heart-pang; Breast-pang .) 

Angina pectoris is a disorder usually associated with sclerosis of the 
first portion of the aorta and the coronary arteries, and characterized 
by paroxysmal attacks of excruciating pain in the region of the heart, 



494 DISEASES OF THE ARTERIES 

a sensation of constriction of the chest, and a feeling or fear of impending 
death, and sometimes sudden death. 

Etiology. — Angina pectoris is a disease of adult life (after the fortieth 
year) and of the male sex; women are very rarely affected. The etio- 
logical factors are those of arteriosclerosis, especially alcoholism, syphilis, 
chronic nephritis, gout, excessive muscular and mental work, etc. 

Pathology. — The lesions found in fatal cases consist of sclerosis and 
atheroma of the first part of the aorta, of the coronary vessels (especially 
their mouths), and of degenerative (fibroid and fatty) changes of the 
myocardium. Often there is associated disease of the aortic valve and 
orifice, or aneurysm of the aorta. In some cases degenerative changes 
have been found in the cardiac ganglia. Rarely the disorder is found 
in association with mitral disease. In a few cases no noteworthy lesions 
have been found (perhaps they have been overlooked). 

The nature of the disease has not been fully elucidated. It is assuredly 
absurd to describe it as a neurosis, as is commonly done. Clifford 
Allbutt, with much reason, regards the disorder as a painful lesion of 
the first part of the arch of the aorta: an aortitis, rheumatic or influ- 
enzal, etc. (in which cases the tensile stresses may be about or even below 
normal), or atheroma of the aorta (in which cases the tensile stresses 
may be normal or excessive). He believes that sometimes the disorder 
is produced by stretching of the pericardium, as in aneurysm of the 
left ventricle, or by inflammation of that part of the tunic which invests 
the root of the aorta, and that very rarely it may depend on some extraor- 
dinary kind of disturbance in the mitral area. Mackenzie points out 
that the symptoms occur in patients with the most diverse forms of 
lesions, even in the absence of any evidence of cardiac disease: the most 
common conditions are aortic aneurysm, aortic valvular disease, atheroma 
of the coronary arteries, myocardial degeneration or enfeeblement from 
poor nourishment or overexertion, and increased arterial pressure 
usually associated with coronary sclerosis and myocardial degeneration 
in elderly subjects. He further points out that in these conditions angina 
pectoris is a late symptom, developing after the heart has been struggling 
for a long time against obstacles opposed to an efficient action, or after 
the nutrition of the muscle has been impaired by gross pathological 
changes in the coronary artery, or when the myocardium has become 
impaired through slowly advancing degeneration of the muscle fibers; 
that many patients when at rest do not suffer from pain, but that any 
cause inducing increased work in the heart provokes an attack. He 
concludes that angina pectoris is an evidence of exhaustion of contrac- 
tility, and occurs when the contraction meets a greater resistance than it 
can easily and efficiently overcome, whether a fairly strong muscle 
struggles against an increased resistance, or when a weak or degenerated 
muscle has opposed to its contraction a normal or even lowered pressure, 
but a pressure greater than the weakened muscle can readily overcome. 
Huchard attributes the attack to anemia of the heart muscle the result 



ANGINA PECTORIS 495 

of disease or spasm of the coronary arteries, and compares it to inter- 
mittent lameness or claudication. 

Symptoms. — The chief manifestation of angina pectoris is paroxysmal 
pain; but excluding the rare cases of sudden embolic plugging of the 
coronary artery, this paroxysmal pain occurs only after a long period 
of gradual enfeeblement of the myocardium, and it is almost always 
induced by some extra demand upon the heart, such as muscular effort, 
mental excitement, increased peripheral resistance (chilling of the 
surface, etc.), flatulence, etc. The paroxysms may vary considerably 
in severity, from slight precordial pain or constriction of the chest to 
the most severe attacks. These consist of paroxysms of excruciating 
pain in the region of the heart, a sensation of constriction of the chest, 
especially in front, and a feeling of exhaustion and mental anguish 
amounting to an apprehension of impending death. The pain is usually 
of the most excruciating character; it irradiates from the cardiac plexus 
behind the aorta along the distribution of the first four thoracic and the 
seventh and eighth cervical nerves, that is, to the left shoulder, arm, 
and neck; rarely also to the right side, or the abdomen. The associated 
sensation of tightness or constriction of the front of the chest is attrib- 
uted by Mackenzie to spasm of the intercostal muscles induced by reflex 
stimulation. Phenomena of vasomotor disturbance are usually present, 
such as pallor (occasionally flushing) of the face, profuse perspiration, 
etc. The patient may be absolutely immobile, with a staring countenance, 
completely conscious, but unable to articulate; or he may be restless 
and anxious; in either event he is usually overcome emotionally by the 
greatest mental anguish. During the attack the heart is variable; often 
it reveals no changes aside from the phenomena of arteriosclerosis, being 
quite normal in rate, rhythm and strength; but the pulse may become 
soft, compressible, and scarcely perceptible (weak heart), or extra- 
systoles and the alternating pulse may occur. Mackenzie states that the 
blood pressure may not be increased. Dyspnoea is not a phenomenon 
of angina pectoris per se, although it may be induced by associated 
conditions. The attack lasts from a few seconds to a minute or there- 
abouts; rarely, however, severe pain or a succession of attacks may con- 
tinue for an hour or more. The paroxysm may lead to immediate 
death (even the first paroxysm), or it may subside as suddenly as it 
began, or at its height the patient may pass into syncope. The end 
of the paroxysm may be associated with the eructation of gas (uncon- 
sciously sucked in during the attack), the passage of a large amount of 
urine, etc. After the attack the patient feels exhausted for several hours 
or several days, and some substernal distress may persist for a short time. 

Recurrences may ensue for several days in succession with increasing 
weakness of the myocardium; or at irregular, more or less long, intervals, 
over a period of years; or the first may prove to be the only attack. 
Cessation of the attacks may follow dilatation of the heart and relative 
mitral insufficiency (Musser), but the ordinary signs of decompensation 
are likely soon to supervene. 



496 DISEASES OF THE ARTERIES 

Diagnosis. — The severe paroxysms are sufficiently characteristic as 
scarcely to be mistaken. Slight attacks are often overlooked or mis- 
interpreted, but it is significant if they are provoked by exertion, excite- 
ment, etc., and if they are associated with anginoid attacks in the legs 
(intermittent lameness), or in the gastro-intestinal tract (abdominal 
angina) etc. The so-called pseudo-angina that occurs in hysterical, 
neurasthenic, and other nervous disorders must be excluded. Huchard 
points out that it is most common in women of all ages; the attacks 
are spontaneous, and often periodical and nocturnal; the pain is less 
severe, lasts a long time, and is associated with other nervous phenom- 
ena — vasomotor and neuralgiform; it is not fatal; and it is improved 
by medication directed to the nervous system. A toxic angina is some- 
times set up by tobacco, coffee, etc. Nothnagel described a vasomotor 
angina, characterized by coldness and numbness (vasomotor spasm) 
of the extremities, faintness, and precordial pain. 

Prognosis. — The condition, of course, is grave, but not so apprehen- 
sively so as is often maintained; it depends upon the efficiency of the 
heart muscle, and the care with which the patient regulates his life. 
While the first attack may be, it is usually not, fatal, and proper treat- 
ment may lead to cessation of the attacks. 

Treatment. — The treatment in general is that of arteriosclerosis 
and the fibroid heart, the chief indications being to reduce the pressure 
against which the more or less exhausted myocardium must contend, 
or the stress or tension to which the sore aorta (Allbutt) is subjected, 
and to avoid all the factors that may provoke an attack. Underlying 
conditions such as rheumatism, gout, syphilis, diabetes, flatulence, etc. 
must receive appropriate treatment. The patient must bring his daily 
work well within the capabilities of his heart; he must avoid all over- 
exertion, and lead a quiet life. A prolonged holiday or a course of 
treatment at some one of the well-known spas is often very efficacious. 
In some cases rest in bed for a time is essential. The diet must be 
restricted and carefully regulated, an excess of meats and especially of 
carbohydrates being avoided, especially at the evening meal; and cardiac 
excitements, such as alcohol, coffee, tea, tobacco, must be prohibited. 
The frequent use of mercurial and saline laxatives is very valuable. 
The iodides seem to be of unquestionable service; potassium, sodium, 
or ammonium iodide should be given in small (3 to 5 grain, 0.2 to 0.3 
gram) doses for a long time, with short periods of intermission (one week 
in four) ; or one may use nitroglycerin for the physiological effect, in fre- 
quently repeated doses (since the effect of each dose does not last more 
than an hour); or one may give erythrol tetranitrate (J grain, 0.03 
gram, three or four times daily), or the nitrites — which have a more 
lasting effect. 

The paroxysms are best treated with amyl nitrite, of which 3 to 5 
minims (0.2 to 0.3 gram) should be given by inhalation. A subject of 
angina pectoris should carry glass capsules or perles containing the men- 
tioned dose ? and immediately upon the onset of the paroxysm break one 



ANEURYSM 497 

in his handkerchief and inhale it; relief is usually prompt and complete. 
In some cases benefit does not ensue, in which event resort should be 
had to morphine (J grain, 0.015 gram) and atropine (-j-g-g- grain, 0.0006 
gram) hypodermicly; or, as recommended by Osier, a few whiffs of 
chloroform (it must be used with caution, since it may prove a dangerous 
remedy). Recurring nocturnal attacks may be sometimes prevented by 
chloral, the bromides, valerian, etc. Allbutt recommends the continuous 
use of atropine, in increasing doses as tolerance is established, with a 
view to blocking the impulse by which the heart is inhibited. The 
treatment of the eventual failure of the heart is that of the fibroid 
heart; digitalis, however, as a rule, and similar cardiac tonics are dis- 
tinctly contra-indicated. 

ANEURYSM. 

An aneurysm is a circumscribed tumor containing fluid or solid blood, 
communicating directly with the canal of an artery, and limited by the 
tunic which is called the sac (Hilton Fagge). 

Etiology. — The causative factors in general are those of arteriosclerosis, 
of which aneurysm is a result. Major significance attaches to syphilis 
and excessive muscular strain, whence aneurysms are most common 
in the male sex (86 per cent, of the cases). They develop most commonly 
between the thirtieth and the fortieth year, that is, they " coincide with 
that time of life when the period of greatest bodily vigor overlaps the 
beginnings of the period of the occurrence of atheroma" (Coats). 

Pathology. — True and false aneurysms may be distinguished, the true 
aneurysm being one in which the aneurysmal sac consists in whole 
or in part of the wall of the bloodvessel, the false being one in which 
the aneurysmal sac consists of connective tissue, the wall of the blood- 
vessel having ruptured and permitted the extravasation of blood into the 
surrounding connective tissue; but one must bear in mind that the sacs 
of many so-called true aneurysms in their later stages, at least, are com- 
posed largely of Connective tissue, the walls of the bloodvessel originally 
constituting the sac having become atrophic, degenerated, and replaced 
by newly formed connective tissue. A true aneurysm may be, and 
usually is, circumscribed and saccular, that is, it communicates with 
the lumen of the vessel by a narrow opening called the neck; or it 
may be ectatic, that is, merely a dilatation of the vessel, and fusiform, 
cylindrical, or cirsoid in shape; or it may be dissecting, that is, the 
result of rupture of the intima and consequent infiltration of the 
blood between the coats of the vessel, whence it may find its way into 
the lumen of the vessel again or outward into the adjacent connective 
tissues. Quoting Coats, an aneurysm may be said to be the result of 
"a local disproportion in the normal balance between the amount of 
lateral pressure inside the artery and the elastic resistance of the vas- 
cular walls, arising either from abnormal increase of the former or 
diminution of the latter; most frequently, indeed, from both these causes 
32 



498 DISEASES OF THE ARTERIES 

combined." The increased pressure is a qoncomitant and causative 
factor of the arteriosclerotic process; the diminution in the elastic 
resistance of the vessel is also part of the arteriosclerotic process, but the 
local predisposition that determines the site of the aneurysm is a con- 
genital inherent localized weakness of the vessel wall, or an acquired 
deficiency of vitality that may be only a special localization of the 
sclerotic process or the result perhaps of some infection passed through 
in early life. 

Saccular aneurysms may be single or double (rarely multiple); and 
very small, scarcely more than a slight bulging or pouching of the vessel, 
or they may attain the size of a child's head. Seventy-five per cent, of all 
aneurysms involve the thoracic aorta, and of these, 59 per cent, the 
ascending portion of the arch, 29 per cent, the transverse portion of the 
arch, and 12 per cent, the descending portion (Crisp). 

Rarely other types of aneurysms occur, such as : embolic and mycotic 
aneurysms due to mechanical or infected emboli (they are usually mul- 
tiple); a traction aneurysm on the under surface of the aortic arch, at 
the site of the insertion of the remnant of the ductus Botalli; an arterio- 
venous aneurysm, in which a communication is established between an 
artery and a vein; should the communication be direct the condition 
is spoken of as an aneurysmal varix ; should a sac intervene, it is termed 
a varicose aneurysm. 

Symptoms. — An aneurysm may be for a long time latent; indeed, the 
first manifestations may be the fatal rupture and hemorrhage. In most 
cases, however, sooner or later, manifestations develop, in the one case 
subjective, the aneurysm of symptoms; in the other case objective, the 
aneurysm of physical signs. The symptoms are all pressure effects. 
Pain is most significant; although absent in some cases, it may be the 
most obtrusive manifestation of the disease. It is most likely to be pres- 
ent in deep-seated aneurysms, and is usually described as sharp and par- 
oxysmal, or dull and boring. Persistent pain beneath the sternum, or 
in the region of the fourth, fifth, or sixth thoracic vertebra?, is extremely 
significant, especially if it be unrelieved by medication. Pressure on 
the intercostal nerves may give rise to the most intractable neuralgiform 
pain, which may be referred to the front of the chest, and be for some 
time the only symptom. 

In a majority of the cases the most noteworthy pressure signs are 
connected with the respiratory tract, of which the most important 
are a characteristic cough, alterations in the voice, and dyspnoea, 
due to paralysis or spasm of one or both vocal cords, occasioned 
by pressure on the recurrent laryngeal nerve or nerves, generally 
the left. The cough is brassy, metallic, clanging, or ringing in char- 
acter — a laryngeal cough, and of itself often permits a presumptive 
diagnosis. The alterations in the voice have been well described by 
Walshe, who says that "the speaking voice may be husky, muffled, 
cracked, and hoarse, or simply weakened, or tremulous and variable 
in pitch, or actually lowered in register/' In some cases complete 



ANEURYSM 499 

aphonia results. Laryngoscopic examination frequently reveals the 
larynx normal except in one respect — the cadaveric position of the vocal 
cord corresponding to the recurrent laryngeal that is paralyzed. In these 
cases the other vocal cord crosses the median line and renders phonation 
possible, but in consequence of unequal tension, unequal vibrations, 
and hoarseness, or a peculiar monotone and inability to reach a high 
note, a falsetto voice develops. Dyspnoea, which is often associated 
with marked stridor that may be inspiratory, or inspiratory and expira- 
tory, and which like the cough is often paroxysmal, is an extremely 
characteristic sign. Sometimes the narrow glottis is still sufficient 
for easy respiration during quiescence, but exertion produces increased 
respiratory demand, and during the effort the paralyzed cords are 
violently drawn downward and inward, with resulting apncea. In some 
cases the trachea, or more commonly one of the bronchi, usually the 
left, becomes compressed, and gives rise to paroxysms of dyspnoea, to 
lessening of the respiratory murmur over a part or the whole of the 
corresponding lung, and perhaps also other signs of compression and 
atelectasis of the lung (diminished expansion, dulness on percussion, 
indefinite signs of solidification, etc.). If the pressure be long continued, 
retention of secretion, fetid bronchitis, and bronchiectasis may result; 
and pressure on the bronchial arteries may lead to gangrene of the lung 
or indirectly to tuberculosis (a not uncommon complication). Aside 
from large and often fatal hemorrhages, small hemorrhages (so-called 
weeping of the aneurysm) may occur, being due to rupture of inflam- 
matory capillaries in the trachea or bronchus at the point of compression, 
or to leakage through the sac that has ulcerated into the trachea or 
bronchus or lung. The trachea may be displaced laterally as well as 
anteroposteriorly, and the normal up and down movements during 
deglutition may be restricted. Tracheal tugging may be elicited — a 
distinct tug or downward traction on the trachea occurring synchron- 
ously with the systole of the heart (Oliver's sign) ; a lateral rather than 
a downward traction is sometimes apparent (Cardarelli's sign). Both 
are most common in aneurysms of the transverse or descending arch of 
the aorta that impinge on the bifurcation of the trachea or the left bronchus. 
A tracheal diastolic shock also may sometimes be detected (Hall's sign). 
Pressure on the oesophagus occasions dysphagia; but it is remarkable 
that in some cases of even large aneurysms the oesophagus escapes. 
Dysphagia may also be due to pressure on the vagus or its oesophageal 
branches, in which event there may be also other manifestations of 
gastro-intestinal disorder — vomiting and diarrhoea, but these are unusual. 
The dysphagia is due to an oesophageal stricture (which it virtually 
amounts to); and it is important to bear in mind that in the event of 
suspected oesophageal stricture a bougie or stomach tube should not be 
passed until the possibility of aneurysm has been excluded; on more than 
one occasion a stomach tube has been inadvertently introduced into an 
unsuspected aneurysm. Pressure on the thoracic duct may occur, and 
lead to emaciation; whence it may be difficult to determine whether 



500 DISEASES OF THE ARTERIES 

emaciation is due to such pressure or to oesophageal obstruction and 
the ingestion of insufficient food. 

The aneurysm may be so situated as to interfere with the blood 
supply to one arm or one side of the neck and head. At times this 
results from direct pressure on the supplying artery; in other cases 
it results from the artery springing from the aneurysmal sac, the 
blood supply of the part in question being compromised by the blood 
being obliged to pass through a sac more or less filled with blood clot. 
Examination of the corresponding arteries of the two sides of the arm, 
head, and neck may disclose retardation and weakness or lessened 
volume of the pulse on the affected side; but one must bear in mind 
anatomical differences in corresponding arteries. As pointed out by 
Osier, in some cases of large saccular aneurysm the normal pulse in the 
abdominal aorta and its branches (femorals, etc.) may be obliterated. 
At times, although scarcely as frequently as in intrathoracic tumor, 
obstruction to the venous circulation occurs — congestion and swelling 
of the veins, cyanosis, and sometimes oedema, corresponding in situation 
and extent to the situation and degree of the venous obstruction. In 
some cases more or less well-marked evidences of a vicarious collateral 
circulation appear in the normally small veins beneath the skin. Club- 
bing of the finger ends and incurving of the nails, usually unilateral and 
corresponding with that toward which the pressure of the aneurysmal 
sac is directed, have been observed in some cases. 

Pressure on the ciliospinal branches of the sympathetic nerve is by no 
means uncommon. Should it be moderate, sufficient only to irritate or 
stimulate the vasodilator fibers, dilatation of the pupil and pallor of the cor- 
responding half of the face result; should the pressure be sufficient to para- 
lyze or destroy the vasodilator fibers, the pupil becomes contracted, and the 
half of the face hyperemic and the seat of increased perspiration. In some 
cases there may be narrowing of the palpebral fissure and enophthalmos. 
Exophthalmos has been observed; it has been attributed to retrobulbar 
venous engorgement, but it is inexplicable in some cases (perhaps stimu- 
lation of the unstriped orbital muscle attached to the eye ball). 

Physical Signs. — The important physical signs consist of a visible 
and palpable abnormal expansile pulsation, usually to one side of or 
beneath the sternum, or in the episternal notch, or in the left back or 
axilla. Over the pulsation a thrill, usually systolic, occasionally also 
diastolic, may be palpable; a diastolic shock is common, and is due 
sometimes to augmented recoil of the aortic leaflets (when the valve 
is competent), sometimes to recoil of the aneurysmal sac or the aorta 
between the sac and the aortic valve. The aneurysm occasions an area 
of dulness which usually merges with the cardiac dulness; this dulness 
is of the greater significance the farther it extends from beneath to either 
side of the sternum in the first, second, or third intercostal space. Dul- 
ness may be found also posteriorly, usually beneath or to the left of the 
vertebrae. In deep-seated aneurysms no dulness may be elicited; and 
in other cases the dulness may be obscured by co-existing emphysema. 



ANEURYSM 501 

Auscultation may reveal no abnormalities. In the majority of cases, 
in the early stages at least, two sounds are audible over the aneurysm 
— the two sounds heard normally in the aortic area. Some observers 
attribute the second sound to the aneurysm itself, which perhaps may be 
the case in associated aortic insufficiency, in which, however, a second 
sound may not be heard either at the aortic area or over the aneurysm. 
In some cases a systolic murmur is audible over the sac; in other cases 
a double, systolic and diastolic, murmur; the diastolic murmur may be 
produced in the aneurysm or it may be due to a commonly associated 
aortic insufficiency. The murmur may be audible in the trachea or in 
the open mouth of the patient. The heart is, as a rule, more or less 
displaced, and commonly reveals the physical signs of more or less 
hypertrophy, which is due to the associated arteriosclerosis, aortic valve 
disease, etc. ; the aneurysm as such produces little if any hypertrophy. 

Diagnosis. — The diagnosis depends in part upon the symptoms, and 
in part upon the physical signs. The association of an otherwise in- 
explicable cough, dyspnoea, and interthoracic pain should always 
awaken the suspicion of deep-seated aneurysm. Percussion and palpa- 
tion of a localized area of the anterior chest may provoke paroxysms 
of severe pain and coughing, which Eichhorst believes significant of 
aneurysm. Aneurysms of the ascending aorta usually grow from the 
anterior surface forward and to the right, and present in the first, second, 
or third right intercostal space, and produce, as a rule, obtrusive physical 
signs. Aneurysms of the transverse arch usually grow from the con- 
cavity of the arch downward and backward; symptoms rather than 
physical signs are likely to be obtrusive, although dulness may be found 
beneath and to the left of the sternum, or in the back. Aneurysms 
of the descending arch are likely to grow from the posterior surface, 
and to be for a long time latent or to produce indefinite or ill-defined 
symptoms. In all cases of aneurysm, the most conclusive diagnostic 
aid is furnished by the use of the arrays. 

In the differential diagnosis one must exclude other forms of pulsation, 
such as the so-called dynamic pulsation, which is common in the aorta 
in cases of aortic insufficiency, and in the abdominal aorta; even wide- 
spread and forcible pulsations of this sort often subside remarkably 
under the influence of rest. The palpable pulsation of the abdominal 
aorta common in thin and neurotic individuals is all too commonly 
interpreted as an abdominal aneurysm. The diagnosis of an aneurysm 
of the abdominal aorta depends upon the detection of a definite palpable 
expansile tumor. Pulsating empema in the neighborhood of the heart 
should not occasion any diagnostic difficulty. Most difficulty is experi- 
enced in distinguishing between an aneurysm of the aorta and a solid 
mediastinal tumor; but aneurysm is most common in males, between 
the ages of thirty-five and fifty-five, especially those who have been 
engaged in laborious occupations, who have become infected with 
syphilis, and who have used alcohol to excess; intrathoracic growths 
exhibit no special predilection for either sex; they occur at any age 



502 DISEASES OF THE ARTERIES 

if secondary, but usually before the age of thirty-five if primary, and 
occupation, alcohol, and syphilis (except in cases of gumma) are without 
etiological significance. A bulging expansile tumor is pathognomonic 
of aneurysm; in the case of intrathoracic tumor, a primary growth 
elsewhere in the body or the development of a mass of enlarged lymph 
nodes above the clavicle is likewise practically pathognomonic. (Edema 
of one side of the chest, especially if unassociated with oedema of the 
corresponding arm, is suggestive of tumor. A systolic or a double 
murmur, if unassociated with other evidence of valvular disease, is 
suggestive of aneurysm; murmurs, as such, have no relation to intra- 
thoracic growths, but they may develop if the heart be displaced or the 
bloodvessels be encroached upon or distorted. A palpable diastolic 
shock and a marked accentuation of the aortic second sound is quite 
common in aneurysm, but usually absent in tumor. Tracheal tugging 
does not occur in tumor, although a slight systolic movement of the 
trachea (observable even in some healthy persons) may be detected. The 
effects of aneurysm on the lung are usually those of compression only, 
whereas the effects of tumor growth may be manifest by solidification, 
the growth invading the lung tissue and in some cases giving rise to 
metastatic nodules. In the case of tumor a clear, or probably more 
likely a blood-stained, fluid is common when the growth has reached 
and invaded the pleura; should an aneurysm give rise to alterations in 
the pleura, acute pleuritis usually results. Pain is usually less severe, 
and is certainly less characteristic in tumor formation than it is in aneu- 
rysm, although it may be entirely absent in some cases of aneurysm. 
Pressure effects on the recurrent laryngeal nerve are more suggestive 
of aneurysm than of tumor. Under the influence of rest, potassium 
iodide, and other treatment, the symptoms of aneurysm usually, for 
a time at least, show amelioration, whereas almost without exception the 
symptoms of tumor are continuously progressive. The course of aneu- 
rysm is very variable and it may last for years, whereas intrathoracic 
growths almost certainly result fatally within a year from the onset of 
symptoms. 

Prognosis. — The outlook in aneurysm is bad, since from the nature of 
the disease the outcome is necessarily fatal; occasionally a spontaneous 
cure results. The usual duration of life after the diagnosis has been 
made is from two to three years, although it may be prolonged 
by appropriate treatment. Death usually (75 per cent, of the cases) 
results from rupture and hemorrhage into the pleura, the pericardium, 
the trachea, a bronchus, the oesophagus, or externally after erosion 
and perforation of the sternum and the adjacent costal cartilages or 
ribs. Death may be due also to asphyxia from compression of the trachea 
or a main bronchus, to inanition from compression of the oesophagus 
of the thoracic duct, to embolism especially of the brain, etc. 

Treatment. — The main object of treatment is to promote clotting 
within the sac and consequent cicatrization. These are best achieved 
by rest and a restricted diet (so-called Tufnell treatment), which reduce 



ANEURYSM 503 

the force and frequency of the heart beat. The rest should be absolute 
in bed for two or three months, and should be combined with mental 
quietude and freedom from excitement and worry. The diet should 
be reduced to a minimum : Tufnell advised only ten ounces of solids and 
eight ounces of fluids — a regimen which is scarcely necessary, and if 
rigidly insisted upon usually induces the patient to seek another physi- 
cian. After the early rest in bed, if the patient has submitted to it, 
he should be directed to lead an orderly and quiet life, the danger that 
threatens, on excitement, exertion, and augmented blood pressure being 
pointed out to him. His bowels should be moved freely daily with laxa- 
tives, so as to avoid the straining inevitable in constipation. The iodides 
(30 to 60 grains, 2 to 4 grams, daily), continued for a long time, unques- 
tionably do good in many cases, the syphilitic as well as the non- 
syphilitic; usually they notably mitigate the pain, and in some cases 
they seem to promote clotting within the sac. Calcium lactate (40 to 60 
grains, 2 to 4 grams, daily) may be given for four or five days from 
time to time with the same object in view. Gelatin is thought also to 
promote clotting, and may be given with the food, but its value, aside 
from the contained calcium, is doubtful. Pain may be somewhat relieved 
by hot or cold applications, counterirritation, etc., but it is sometimes 
so severe as to demand morphine, which from the nature of the disease 
need not be withheld from time to time, although it should be used 
with circumspection. Aconite is sometimes of service in quieting an 
overactive heart. The introduction of gold wire and electrolysis to 
promote rapid clotting has been successfully performed in a number of 
cases, with relief to the patient's suffering and prolongation of his life. 
Obviously it should be employed only in sacculated aneurysms. 



SECTION VII. 
DISEASES OF THE BESPIRATORY SYSTEM. 



Pathological Physiology. — The respiratory system is designed to sub- 
serve the function of gaseous exchange between the body and its environ- 
ment; that is, the absorption by the blood circulating in the pulmonary 
capillaries of oxygen from the air contained within the j ulmonary alveoli, 
and the giving up by the blood to the air of carbon dioxide. This, the 
so-called external respiration, is much related to and upon it depends the 
so-called internal respiration — that is, the gaseous exchange that takes 
place between the blood and the tissues, the absorption by the tissues 
of oxygen essential to their vital, or metabolic, activities, and the giving 
off into the blood of carbon dioxide, one of the end-products of katabo- 
lism. The lungs, therefore, are primarily concerned in the oxidative 
processes, of w r hich the metabolic and nutritive processes largely consist; 
and the life history of the oxygen taken into the body by way of the 
lungs (to a limited extent also by the skin) soon becomes associated 
with that of the food taken in by way of the digestive system; but this is 
a subject that pertains more to disturbances of nutrition than of res- 
piration. 

The lungs are prevented from collapsing by the pressure of the atmos- 
phere (15 pounds to the square inch) which reaches the lungs by way 
of the air passages and cannot exert a compressing force on the lungs 
from without, on account of the resistance of the bony and muscular 
framework of the thorax. In conditions of deficient entrance of air into 
the lungs considerable depression of the intercostal spaces may occur 
(especially noticeable in children with laryngeal or tracheal obstruction) ; 
and should the bony framework of the chest become softened (as in rickets) 
notable deformity may and usually does ensue. In the event of perfor- 
ation of the chest wall and the consequent access of the air to the pleural 
sac, the lung collapses, usually to about one-fifth its normal volume; this 
is due not only to the atmospheric pressure as such, but also to over- 
coming of the normal negative intrapleural pressure (4 to 6 mm. Hg.), 
and to the activity of the contractility of the lungs. The contractility 
of the lungs is the resultant of the large amount of elastic tissue in the 
pulmonary parenchyma and of the musculature of the bronchi; these, 
when normal, give the lungs their normal tone and are the basis upon 



506 DISEASES OF THE RESPIRATORY SYSTEM 

which normal pulmonary percussion resonance depends. This con- 
tractility of the lungs, as well as the negative intrapleural pressure that 
it occasions, is of much importance in disease; it may become impaired 
from overstrain by increased intrapulmonary pressure (blowing wind 
instruments, etc.) and by disease of the elastica, as happens in emphysema, 
as well as by compression of the lung by a collection of fluid in the 
pleura, or extensive disease (such as pneumonia) of one lobe; in all of these 
conditions the percussion note becomes vesiculotympanitic in character. 
The contractility of the lung on the non-diseased side also is a factor in 
causing displacement of the heart and mediastinum in conditions, such 
as pleural effusion or transudation and pneumonothorax, in which the 
one lung becomes more or less collapsed; and the negative intrapleural 
pressure is doubtless a factor in inducing hydrothorax when the pleural 
vessels become passively congested (chronic cardiac and pulmonary 
disease). 

Both phases of respiration, inspiration and expiration, result from 
muscular activity, notably of the scaleni and intercostal muscles and the 
diaphragm; both are due to the rhythmically recurring activity and relax- 
ation of the opposing sets of muscles. While expiration is almost unop- 
posed, during inspiration the contractility of the lungs, the elastic resist- 
ance of the chest wall, and the force of gravity (represented largely in the 
bony framework of the thorax) must be overcome. How irrational, then, 
in diseased states to add to the embarrassment of an already embarrassed 
respiration by the use of heavy bedclothes, a heavy poultice to the front 
of the chest, etc. During inspiration the lungs expand downward, 
forward, and laterally, the greatest excursion occurring downward and 
laterally, whence the friction sound of pleuritis is usually best heard in 
the anterolateral aspect of the chest. Comparatively little expansion 
occurs upward or backward; such expansion upward as does occur 
is due largely to descent of the lungs as a whole, a fact in part, at least, 
answerable for the common localization of tuberculosis at the apices. 

The normal vital capacity of the lungs, that is, the greatest volume 
of air that can be expired after the fullest possible inspiration, varies 
between 3500 and 4000 c.c, averaging in the adult male about 3700 c.c. 
(Howell). It varies somewhat with the size of the chest, the age and 
height of the individual (being greater in tall than in short subjects); 
it is less in the prone than in the sitting or upright posture (whence the 
exaggerated dyspnoea of the prone posture). It diminishes in old age, 
in part on account of ossification of the costal cartilages and rigidity of the 
thorax, and it is reduced in diseases of the lungs, especially tuberculosis. 

The tidal air, the air breathed in and out during ordinary quiet 
respiration, averages about 500 c.c. ; the complemental air, the amount, 
in addition to the tidal air, that can be breathed in by the fullest possible 
inspiration, averages about 1600 c.c; and the supplemental air, the 
amount which by a forced expiration can be breathed out after an ordi- 
nary quiet expiration, averages also about 1600 c.c. The tidal air, the 
complemental air, and the supplemental air together make up the 



PATHOLOGICAL PHYSIOLOGY 50? 

vital capacity. The residual air, the amount of air that remains in the 
lungs after a forced expiration, averages about 1000 c.c; it becomes 
much increased in emphysema. In health and during normal breathing 
the reserve supply of air amounts to about 2600 c.c, that is the supple- 
mental air plus the residual air. Of the 500 c.c. of air regularly inspired 
during quiet breathing, about 360 c.c. (Howell) reaches the pulmonary 
alveoli by a process of diffusion; this bears a relation to the reserve supply 
of air about as 1 to 7, so that one may assume a renewal of the air 
contained within the lungs once during each seven or eight respiratory acts. 

The tidal air suffices for the ordinary requirements of life, but the 
increased demand for oxygen entailed by muscular exercise is met by 
deep breaths (supplemental air) and increased frequency of breathing. 
Similarly in diseased states, when the available breathing surface of the 
lungs becomes lessened or the blood surcharged with carbon dioxide, 
deep and frequent respirations (dyspnoea) are obvious efforts on the 
part of the body to supply a sufficiency of oxygen; this is not always 
successful, so that to the dyspnoea, cyanosis is added. In a healthy man 
weighing 70 kilograms (150 pounds) the average daily intake of oxygen 
is about 700 grams, and the average daily output of carbon dioxide is 
about 800 grams. This may be increased by excessive muscular activity 
and other factors. 

The composition of the inspired air averages, in volume per cent., 
nitrogen, 79; oxygen, 20.96; and carbon dioxide, 0.04; and the expired 
air, nitrogen, 79; oxygen, 16.02, and carbon dioxide, 4.38 (Howell). 
This gain of 4.34 volumes per hundred of carbon dioxide and loss of 4.94 
volumes of oxygen does not accurately represent the change in the 
composition of the air in the alveoli, since during ordinary quiet respira- 
ation only 72 per cent, of the tidal air reaches the alveoli. In the alveoli 
the carbon dioxide reaches 5 to 6 volumes per cent., and the oxygen 
falls to 13 to 14 per cent. Furthermore, the air as expired has been 
warmed almost, if not quite, to the body temperature, whereby the 
body loses daily from 50 to 100 calories; and the expired air is also almost 
saturated with aqueous vapor, from 250 to 500 grams of water being 
thus lost, and in consequence of the evaporation entailing a daily loss of 
from 145 to 290 calories. In addition, the expired air is often said to 
contain a poisonous, volatile, organic substance to which the ill effects 
(headache, depression, etc.) of the vitiated atmosphere of badly ventilated 
rooms, churches, schools, and other places where large numbers of 
people congregate, are attributed. The results of investigations of this 
subject are not entirely conclusive, but there is no definite proof of the 
existence of such a poisonous organic substance. The unquestionable 
ill effects of bad ventilation are with more propriety attributed to decrease 
of oxygen, increase of carbon dioxide, augmented temperature of the air 
and its saturation with aqueous vapor, and exhalations from unclean 
bodies, perspiration, excretions from the sebaceous glands, and odors 
from clothes. 

The normal body is able to withstand the effects of considerable 



508 DISEASES OF THE RESPIRATORY SYSTEM 

variations in atmospheric pressure without ill consequences; but this 
varies much in different individuals, and is considerably reduced in 
diseases of the lungs and the heart and bloodvessels. Notable reduction 
in atmospheric pressure, such as obtains at high altitudes (mountain 
climbing, balloon and aeroplane ascents, etc.), often results in so-called 
mountain sickness (weakness, faintness, syncope, epistaxis, etc.); and 
the results of increase in atmospheric pressure are well exemplified in 
caisson disease. Compressed air, however, may be resorted to with 
benefit in many cases of diseases of the lungs. 

The chief results of disease of the respiratory system, in so far as this 
system itself is directly concerned, consist of diminution of the external 
gaseous exchange. This is, in part, a passive, physical process; in part, 
an active vital process, the result of a specific functional activity of 
the alveolar epithelium — which may become deranged or. abolished in 
disease. Speaking generally, this diminished gaseous exchange may be 
due to impeded entrance of air into the lungs or to inability on the part 
of the lungs to utilize an adequate supply of air. In either event the 
obtrusive clinical manifestations consist of: (1) Disturbances in the 
rate and rhythm of respiration, and (2) of cyanosis; but both of these 
phenomena may be due also to disorder of the heart, as well as to other 
factors. 

Disturbances in the Rate and Rhythm of Respiration com- 
prise: 

1. Dyspnoea. The term dyspnoea is generally applied to any note- 
worthy increase in the force, rate, or depth of the respirations; some- 
times it is restricted to labored breathing, being thus distinguished from 
merely quickened breathing (hyperpncea, polypncea, tachypncea), a 
condition that may be observed after muscular exercise, during nervous 
excitement or perturbation, in cerebral disorders, in hysteria, etc. Dysp- 
noea is a provision of nature designed to subserve the function of 
breathing, that is, the proper oxygenation of the blood, and it is the 
consequence of obstacles to the ready performance of this function or 
of increased demands for oxygenation (deficiency of oxygen or increase 
of carbon dioxide, which is a direct stimulant to the respiratory centre). 
It varies in degree in different cases — from slight breathlessness on exer- 
tion or excitement to orthopncea even when the patient is at rest in bed. 
It may be objective or subjective, or both; that is, it may or may not be 
accompanied by subjective sensations of substernal or thoracic distress 
or actual pain, oppressed breathing, lack of air, and more or less anxiety 
and apprehension; in some cases the subjective sensations (so-called 
air-hunger) may entirely overshadow the objective dyspnoea. Although 
increased frequency of the respirations is usually an obtrusive feature, 
increased respirations are not always dyspnoeic, and notable dyspnoea 
may be associated with oligopnoea. Dyspnoea may occur in the following 
conditions: (a) All painful affections of the respiratory tract (including 
the pleura), the thoracic wall, the diaphragm, etc. The respirations are 
likely to be superficial and of increased frequency, (b) Obstruction of 






PATHOLOGICAL PHYSIOLOGY 509 

the upper air passages: obstructions within the lumen, disease of the 
passages themselves constricting the lumen, or compression from without. 
The respirations are likely to be deep, they are often infrequent, there is 
usually an associated inspiratory stridor, and the expiration, as a rule, is 
not prolonged, (c) Obstruction of the lower air passages — the smaller 
bronchi and bronchioles, such as occurs in the several types of bronchitis, 
in bronchial asthma, etc. The respirations are likely to be increased in 
frequency, and there is usually prolonged expiration and expiratory 
stridor, (d) Disorders of the pulmonary alveoli, in which the available 
breathing surface becomes restricted, such as pulmonary congestion and 
oedema (of which unstable or non-compensated cardiac disease is 
usually the primary factor), emphysema, inflammatory conditions 
(pneumonia, bronchopneumonia, abscess, etc.), as well as conditions 
that lead to compression of the lungs (pleural and pericardial collections 
of fluid, pneumothorax, mediastinal tumors, distortion of the vertebrse, 
displacement upward of the diaphragm, etc.). The respirations are 
usually of increased rate, force, and depth, (e) Infectious febrile con- 
ditions generally. The increased respirations are due to a direct action 
of the bacterial toxins and the augmented temperature on the respiratory 
centre and to surcharging the blood with carbon dioxide, a consequence 
of increased metabolism. (/) Intoxications, such as uremia and diabetic 
coma, in which KussmauFs dyspncea, or air-hunger (deep, energetic, 
long-drawn inspirations contrasting with short, sighing expirations), 
may be observed, (g) Anemic conditions, in which the available hemo- 
globin may be so small that even frequent and deep respirations do not 
suffice to satisfy the demand for oxygen. 

2. Oligop?ioea. Infrequent breathing may be regular or irregular 
(arrhythmic). It results from depression of the respiratory centre, and 
may be encountered in — some severe infections; exogenous poisonings, 
such as opium and chloral poisoning; autogenous intoxications, such as 
uremic and diabetic coma; nervous disorders, such as meningitis, hemor- 
rhage and tumor of the brain; and the death agony. 

3. Arrhythmic Breathing. There are two chief types of peculiarly 
arrhythmic breathing: (a) Cheyne-Stokes breathing, which occurs in 
arteriosclerotic subjects (cardiovascular-renal disease), uremia, myocar- 
dial degeneration, conditions of increased intracranial pressure, etc., and 
is characterized by longer or shorter periods of apncea (cessation of 
breathing) alternating with periods of breathing, at first slow and shal- 
low, but gradually becoming deeper and more rapid until they reach a 
maximum, whereupon they gradually decrease and finally again cease; 
and (b) Boit's, or meningeal, breathing (which, however, occurs in condi- 
tions other than meningitis); it is characterized by more or less periodic, 
but sometimes irregularly recurring, pauses in breathing lasting from a 
few to thirty or more seconds, and is unattended by the characteristic 
increase and decline of the respirations of the Cheyne-Stokes breathing. 
The causes of the periodicity of these types of breathing are not well 
understood. Both are of serious prognostic significance. 



510 DISEASES OF THE RESPIRATORY SYSTEM 

4. Asphyxia or Suffocation. Complete obstruction of respiration 
and final cessation of breathing may result from: (a) Subjection to an 
inert or irrespirable atmosphere; (b) obstruction of the larynx or trachea 
by an impacted foreign body, false membrane, tumor, etc., or by com- 
pression from without, as by an aneurysm, mediastinal tumor, goitre, 
etc., or by hanging or strangulation; (c) laryngeal spasm or oedema or 
paralysis of the vocal cords; (d) drowning; (e) inundation of the lungs 
by fluid from within the body — blood (ruptured pulmonary bloodvessel 
or aneurysm), serous fluid (severe, especially acute, pulmonary cedema), 
pus (retropharyngeal abscess, etc.); (/) intoxications, such as accom- 
pany chronic passive congestion from decompensated cardiac disease, 
in which the excess of carbon dioxide poisons the respiratory centre; 
morphine, chloral, or chloroform, which poison the respiratory centre 
directly; and coal-gas poisoning, in which carbon monoxide replaces 
the oxygen from the hemoglobin; and (g) severe and prolonged tetanic 
convulsions (strychnine poisoning, tetanus, status epilepticus). 

Cyanosis. Cyanosis commonly attends dyspnoea and is due to 
like causes, to a deficiency of oxygen and an excess of carbon dioxide in 
the blood. Dyspnoea, however, may occur without cyanosis, as in uremia, 
and cyanosis may be present without dyspnoea, as in congenital heart 
disease. Cyanosis is common in diseases of the lungs interfering with 
proper oxygenation of the blood, and may result from obstruction to 
the entrance of air into the lungs, to restriction of the available breathing 
surface of the lungs, and to weakness of the respiratory muscles and 
nerves. It occurs also in disease of the heart, in erythremia (page 385), 
in chronic acetanilide and other coal-tar poisonings, and in so-called 
enterogenous cyanosis (page 414). 

There are a number of acts, such as coughing, sneezing, sighing, 
yawning, sobbing, hiccough, etc., that may be looked upon as modified 
respiratory movements. Coughing, the most important of these, is 
primarily and essentially protective in character, being designed to rid 
the upper air passages of irritating bodies or particles or fluid secretions; 
it may also be produced by irritating vapors, and by stimuli originating 
in various parts of the body and communicated to the pneumogastric 
nerve. The chief sources of such stimuli comprise the larynx, the 
posterior aspect and the bifurcation of the trachea, and the pleura. So- 
called gastric, hepatic, splenic, and uterine coughs are sometimes 
described, but there is no proof whatever of their acutal occurrence. In 
the event of pathological secretions being present in the air passages, 
coughing subserves the useful purpose of their elimination; it should not, 
therefore, be unwisely suppressed at all hazards, since retained secretions 
are likely to undergo decomposition and may bring in their wake con- 
ditions other than those to which they owe their origin. Often, however, 
it is excessive and disadvantageous, distending the lungs unduly in con- 
sequence of increased intrapulmonary pressure, increasing the intra- 
thoracic pressure and impeding the flow of blood to the heart, and 
subjecting the patient to the danger of rupturing a bloodvessel; in these 



DISEASES OF THE NOSE 511 

cases the cough per se should be kept in control. On the other hand, 
weak or ineffectual coughing or the inability to cough may prove a 
source of danger to the subject, leading to retention of foreign bodies, 
pathological secretions, etc.; this occurs especially in aged and infirm 
persons, in those debilitated from any cause, in muscular asthenia, 
especially of the respiratory muscles, in diabetic, uremic, and other 
forms of coma, in anesthetization, and in grave disorders of the nervous 
system. The retained secretions, being usually infected, commonly lead 
to bronchopneumonia and often a fatal termination. 



DISEASES OF THE NOSE. 



EPISTAXIS. 

(Nose-bleeding.) 

Etiology. — Epistaxis, the most common mucous-membrane hemorrhage, 
may be due to general or local causes. The general causes are those that 
determine hemorrhage in other parts of the body, such as: (1) The acute 
infectious diseases, especially typhoid fever (being characteristic of the 
onset), diphtheria, scarlatina, measles, pneumonia, influenza, etc.; 
(2) blood dyscrasias, such as purpura, scurvy, hemophilia, leukemia, 
pernicious anemia, etc.; (3) conditions of increased arterial tension, 
such as plethora (especially after unusual exertion and suddenly increased 
blood pressure), arteriosclerosis (nose-bleeding of the aged), chronic 
interstitial nephritis, etc.; (4) chronic venous congestion — that of ad- 
vanced cardiac and pulmonary disease, as well as the more local conges- 
tion produced by tumors of the neck, etc.; (5) certain poisonings (phos- 
phorus, salicylic acid, etc.); (6) ascent to high altitudes (mountain 
climbing, balloon ascensions); and (7) it may occur as a manifestation 
of vicarious menstruation. The local causes of epistaxis are commonly 
traumatic — injuries to the nose (fracture of the nasal or cranial bones), 
the presence of foreign bodies, the violent use of instruments, excessive 
"nose blowing," and "nose picking" of children; and local diseases, 
such as acute and chronic rhinitis; diphtheria, tuberculosis, syphilis, 
glanders, and other ulcerative processes; benign and malignant tumors, 
etc. Osier has described a multiple telangiectasis of the skin and mucous 
membrane with recurring epistaxis. 

Pathology. — The bleeding may result from capillary oozing or from 
rupture of the vessel wall (traumatism or ulceration). The frequency 
of this nasal hemorrhage is due to the abundant vascular supply and the 
absence of adequate support to the vessels, which conditions are most 
marked over the middle and inferior turbinate bones, where the veins 
form a well-marked venous plexus. When bleeding is the result of 
local ulceration, it generally comes from an area on the cartilaginous 



512 DISEASES OF THE NOSE 

septum about half an inch from its anterior end. This has sometimes 
been described as the site of predilection. In most cases the hemorrhage 
takes place from only one nostril. 

Symptoms. — Following traumatism the hemorrhage is sudden and 
may persist for some time, or it may cease suddenly. When due to 
fracture of the anterior fossa of the base of the skull, it is usually con- 
tinuous though slight, and is generally mixed with cerebrospinal fluid. 
When due to local causes, it may be sudden, severe, and often very diffi- 
cult to control. When due to general diseases, it may take place on 
the slightest provocation and varies in severity. The blood may be 
arterial or venous. The quantity may vary from a few drops to several 
pounds. It is rarely dangerous to life. 

Diagnosis. — The diagnosis is usually quite evident; but occasionally 
the source of the bleeding may not be immediately apparent. Blood 
from the nasal mucous membrane may be swallowed (especially during 
sleep), and being later vomited, may simulate true hematemesis; or it 
may enter the pharynx and, being expectorated, simulate true hemoptysis. 
Examination of the nasal mucosa and attention to the associated phe- 
nomena should prevent diagnostic errors. 

Prognosis. — The prognosis depends altogether upon the cause of the 
bleeding and the general condition of the patient. 

Treatment. — In most cases the hemorrhage ceases spontaneously. 
Should this not occur, the nasal cavities should be examined to determine 
the seat of the bleeding. Divers sorts of local applications are often 
effectual — adrenalin chloride, hot water, ice water, cocaine, alum, zinc, 
hamamelis, tannin, iron perchloride, etc. Persisting hemorrhage from 
a ruptured vessel may sometimes be stilled by the direct application of 
chromic acid, the Paquelin cautery, etc. Should these measures prove 
ineffectual, the nares should be plugged (anteriorly, posteriorly, or both) 
with cotton or similar material, or a thin rubber finger cot may be 
introduced into the nares and then distended with air or water. Internal 
remedies are of little value, except perhaps calcium lactate in certain 
general disorders associated with lessened coagulability of the blood. 



ACUTE RHINITIS. 

(Acute Coryza; Acute Nasal Catarrh; Common Cold.) 

Etiology. — A "cold in the head" is really an acute infection of the upper 
air passages; it may be merely an acute rhinitis, or the catarrhal inflam- 
mation may extend to the pharynx and perhaps involve the entire upper 
respiratory tract. It may occur as an independent disorder, involving 
persons of all ages, especially during the changeable weather of the late 
fall and early spring. It is commonly attributed to exposure to cold and 
damp, but these, as well as divers local disorders (chronic rhinitis, nasal 
polyps, etc.) and general debilitating conditions, act as predisposing 
factors; the exciting cause is doubtless some bacterium. Micrococcus 



ACUTE RHINITIS 513 

catarrhalis is believed to be the cause of most of the cases that exhibit 
infectious (epidemic) characteristics; other cases seem to be due to the 
pneumococcus, the bacillus of Friedlander, Micrococcus paratetragenus, 
Bacillus septus (Bacillus coryzse segmentosus), etc. In some cases acute 
coryza is merely symptomatic— of certain acute general infections, 
such as measles, influenza, pertussis, syphilis, etc., or drug intoxications, 
such as the iodides, the bromides, etc. ; or it may result from the inhala- 
tion of irritating dust or vapors (acids, ammonia, etc.). 

Pathology. — The nasal mucosa is swollen, congested, cedematous, 
and covered with a profuse, clear, alkaline, mucous secretion — which is 
also abundantly discharged through the nares. The lesions may extend 
to the pharynx and the upper respiratory tract generally, the Eustachian 
tubes, the accessory nasal sinuses, etc. After the lapse of several days 
the swelling and oedema subside somewhat, the secretion lessens and 
becomes mucopurulent in character, and gradually ceases entirely. 
Occasionally the nares may be more or less filled and obstructed by a 
fibrinous exudation (fibrinous rhinitis); this is usually due to the diph- 
theria bacillus, but may also be caused by streptococci, staphylococci, 
and pneumococci. 

Symptoms. — The onset, as a rule, is sudden; not infrequently there is 
initial headache and chilliness (rarely a distinct chill), which are soon 
followed by sneezing, a sense of fulness in the nose, embarrassed breath- 
ing (nasal obstruction, often necessitating mouth breathing), general 
malaise, neuromuscular pains in the neck, back, and extremities, fever 
(100° to 101° F.), rapid pulse, and other fever phenomena. At first there 
is very little nasal discharge, but this soon sets in, and usually becomes 
abundant, clear, and watery. The sense of smell and of taste are usually 
obtunded. The inflammatory lesions may extend to the frontal sinuses, 
and occasion severe frontal headache (at the base of the nose); to the 
lacrymal duct, and lead to conjunctivitis and epiphora; to the Eus- 
tachian tube, and cause temporary deafness and tinnitus aurium; to the 
pharynx and induce local pain and soreness and dysphagia ; to the larynx 
and trachea, and cause hoarseness, difficult phonation, and bronchial 
cough, etc. At the end of thirty-six to forty-eight hours, the swelling 
and congestion of the nasal mucosa begin to subside, nasal breathing 
becomes less embarrassed, the discharge becomes lessened in amount 
and mucopurulent in character, and convalescence is established. 

Diagnosis. — The diagnosis, as a rule, is quite obvious. Care should 
be taken to avoid confounding a simple acute rhinitis with the cases 
symptomatic of one of the general infections, such as measles, influenza 
pertussis, diphtheria, etc. 

Prognosis. — The disease usually runs a course of from three to seven 
days, and is usually free from complications. Rarely the accessory 
sinuses, the Eustachian tube, etc., may become seriously affected; or the 
condition (usually from repeated attacks) tends to become chronic. 

Treatment. — In those subject to repeated attacks, local disease of the 
nose should receive attention. A hygenic mode of life may prevent 

. 33 



514 DISEASES OF THE NOSE 

attacks or mitigate their severity — that is, suitable clothing during 
changeable weather, the avoidance of draughts and exposure to wet 
and damp, good ventilation in working rooms and sleeping rooms, 
frequent bathing, exercise, etc. 

Many attacks are mild, do not occasion much distress or incapacitate 
the patient, and soon subside. But if the attack is at all severe, and if 
there is fever, the patient should go to bed for the first twenty-four hours 
at least. The time-honored purge (calomel or blue mass followed by a 
saline), 10 grains (0.6 gram) of Dover's powder, and hot whiskey and 
water (or hot lemonade) still find justification in frequent abortion of 
the attack; it is really good and effective treatment if the patient sweats; 
but he may be made to sweat otherwise, as, for instance, by a Turkish 
bath, which is often very beneficial. The " fulness in the head" and the 
embarrassed nasal breathing may be relieved by preliminary cleansing of 
the nares with an alkaline solution (Dobell's solution) and the use of 
adrenalin chloride (1 to 1000) or cocaine (1 per cent, in liquid albolene), 
or thymol and camphor (each 0.5 per cent, in liquid albolene). The 
adrenalin and cocaine may be followed by unpleasant after-effects (vas- 
cular relaxation and oedema); they should not be used too frequently, 
and assuredly not given to the patient for self medication. The inhala- 
tion of menthol sometimes lessens the local discomfort. In addition, 
relief may be afforded by the following, in a capsule or tablet, every 
two or three hours : 



]$ — Quinine sulphate 2 grains 

Aspirin (or salol) 3 grains 

Atropine sulphate T ^o grain 

Camphor monobromate 1 grain 



13 
20 

0006 
065— M. 



If there is much fever, a mixture such as the following, is often of much 
service : 



1$, — Spirit of nitrous ether 

Spirit of camphor, of each 3 drams 12 

Camphorated tincture of opium 2 drams 8 

Solution of ammonium acetate, sufficient to make . 3 ounces 100 

S. — Two teaspoonfuls (10 c.c.) every three hours. 



00 
00 
00— M. 



A minute dose of tincture of aconite may be added to this mixture if 
the fever is high and there is mnch vascular throbbing. During con- 
valescence from severe attacks the patient should be careful not to 
expose himself to inclemencies of the weather, and he should take a 
tonic. 

CHRONIC RHINITIS. 

(Chronic Nasal Catarrh.) 

Etiology. — Chronic nasal catarrh may be due to repeated attacks of 
acute rhinitis ; some cases seem to be chronic from the beginning, that is, 
the acute passes into the chronic form; other cases are due to specific 
infections, such as tuberculosis, syphilis, etc. Certain of the atrophic cases 



HAY FEVER 515 

(ozoena) are attributed to microorganisms, such as Bacillus mucosus 
ozcenae, Bacillus fcetidus, etc. Anemia and conditions of general debility 
predispose to the disorder. 

Pathology. — Simple, hypertrophic, and atrophic cases may be dis- 
tinguished. In the simple cases the nasal mucosa is swollen and con- 
gested and covered with more or less thinnish mucous or mucopurulent 
exudate. The erectile tissue, especially of the turbinate bones and the 
septum, is especially susceptible to the action of irritants, including cold, 
and, becoming swollen, may occasion more or less nasal obstruction, 
embarrassed nasal breathing, and consequent mouth breathing. In the 
hypertrophic cases, in addition to the foregoing, there is more or less 
marked and permanent hypertrophy of the nasal mucosa, the forma- 
tion of so-called polyps, and sometimes involvement of the turbinate 
bones, leading to partial or complete obstruction of the nasal passages. 
There is usually also more or less catarrh of the pharynx, with adenoid 
vegetations, and consequent mouth breathing, nasal voice, deafness 
(Eustachian tube involvement), flattened face, peculiar expression, and 
defective mentality (especially when occurring in young subjects); 
perhaps also asthma, bronchitis, etc. The atrophic cases perhaps some- 
times develop out of the hypertrophic, but often they seem to be atrophic 
from the beginning. The mucosa is pale and thin, the erectile tissue 
is atrophic, and both in many places are replaced by ulcerating or scar 
tissue; the nasal passages are widened; there is a little mucopurulent 
secretion, which, drying, forms crusts and occasions an extremely offensive 
odor (ozoena). 

Symptoms. — The chief symptom in the hypertrophic form is embar- 
rassed nasal respiration, which is usually associated with a sense of 
fulness in the nasopharynx, and a more or less abundant mucous or 
mucopurulent excretion, which gives rise to the so-called "hawking" 
and spitting. The atrophic form is especially characterized by the foetid 
odor and more or less local distress. 

Diagnosis. — The diagnosis suggested by the symptoms, is to be made by 
rhinopharyngeal examination. 

Treatment. — The treatment consists of mild antiseptic douches, such 
as DobelPs solution, etc., to insure cleanliness and remove secretions; 
the local use of iodine, potassium iodide, etc., in the hypertrophic form, 
with eventual removal of the enlarged turbinates, and of various anti- 
septics and deodorants in the atrophic forms. For details of the treat- 
ment one should refer to special treatises on rhinology. 

HAY FEVER. 

{Hay Asthma; June Cold; Rose Cold; Autumnal Catarrh.) 

Hay fever is a disease provoked by the pollen of certain grains and 
plants, and is characterized by catarrhal inflammation of the conjunc- 
tiva and the upper respiratory tract, embarrassed respiration (asthma), 
and general depression. 






516 DISEASES OF THE NOSE 

Etiology. — Hay fever is most common in adult males, but it occurs 
in both sexes, especially in those engaged in intellectual as contrasted 
with manual pursuits. Individual sufferers exhibit a special suscepti- 
bility, which it seems may be inherited (familial predisposition), but 
which usually is an acquired general nervous instability or a local 
disorder (hypersensitiveness) of the nerve endings of the nasal mucosa. 
In this country, as well as in England and Germany, the disease begins 
toward the end of May and lasts five to eight weeks; and, especially in 
this country, it appears again about the middle of August and lasts again 
six or eight weeks or until the first frost (which it does not survive). 
Many subjects escape the first, but succumb to the second visitation. 
The exciting cause appears undoubtedly to be the pollen of certain 
grains and plants. Ragweed (ambrosia) and, to a less degree, goldenrod 
(salidago) are the main causes in this country; but grains such as rye, 
(especially in England), corn, etc., and other plants (chrysanthemums, 
asters, etc.) are also of etiological significance. All cases are not pro- 
voked by the one cause; the American disorder, for instance, seems to 
differ etiologically from the English, the German, etc. Dunbar has 
isolated from the pollen a toxalbumin which he believes to be the specific 
cause of the disease; it is pathogenic in susceptible individuals in doses 
of 4 7nro"o milligram. The disease itself is believed to be an expression 
of hypersusceptibility to this toxin, which exerts a specific action on the 
terminal nerve fibers of predisposed persons, and has some influence 
also on the erythrocytes, which it lakes. 

Pathology. — The lesions consist of catarrhal changes in the conjunc- 
tivae and the upper respiratory tract. The asthma and general depression 
are attributable to the general influence of the toxin. 

Symptoms. — The onset, as a rule, is abrupt, and in susceptible subjects 
develops about the same time each year. In many instances the attack 
resembles an ordinary acute coryza, in others, an attack of bronchial 
asthma; or the one may alternate with the other. At the onset, in most 
cases, to the more common manifestations of coryza, there are added 
considerable sneezing, obstructed nasal passages, conjunctivitis with 
marked itching of the eyelids and lacrymation, and severe itching 
sensations of the soft palate and pharynx; the nasal discharge is usually 
copious, thin, and watery — rarely mucopurulent. The catarrhal pro- 
cess may extend to the larynx, bronchi, and lungs, with accompanying 
cough and asthmatic seizures; these may even predominate, and not 
infrequently prevent sleep. Headache, malaise, exhaustion, fugitive 
pains, mental depression, and other general symptoms occur, and there 
may be gastro-intestinal disturbances. Variability in the severity of the 
symptoms may develop from day to day — mitigation due perhaps to 
staying indoors or to rain which precipitates the pollen, and augmenta- 
tion due to going outdoors, especially in the sunshine which dries and 
permits diffusion of the pollen (which may be increased by high winds). 

Diagnosis. — The disease is readily recognized from the rather sudden 
development annually, in the spring, or more commonly in August in 



DISEASES OF THE LARYNX 517 

this country, of severe coryza, accompanied by conjunctival, pharyngeal, 
and bronchial (asthmatic) symptoms, and general depression. 

Prognosis. — The disease usually lasts five to eight weeks and subsides 
spontaneously — the autumnal catarrh with the first frost. Rarely 
a person attacked in the spring suffers more or less throughout the 
summer and until October. Those once attacked are likely to suffer 
again, but spontaneous abatement of the symptoms is sometimes ob- 
served after the age of about sixty years. 

Treatment. — The only certain means of relief is a sojourn, during the 
hay-fever season, at a high altitude in a region free from the ragweed, 
etc. The White Mountains, the Adirondacks, as well as certain moun- 
tainous regions of the South and West and Canada, afford complete 
immunity. Some subjects do well at the seashore. Dunbar has intro- 
duced a pollen antitoxin, under the name of pollantin (marketed in a 
dry and in a liquid form), which is to be used locally in the nose (and 
not injected hypodermicly) ; he asserts that he has employed it with 
excellent results or partial success in 87 per cent, of 1240 cases. Tem- 
porary relief is afforded by the local use of adrenalin chloride (1 to 1000), 
cocaine (whence the habit has often been acquired), menthol, morphine, 
etc., and by the internal use of atropine, which usually produces the 
greatest relief. S. Solis-Cohen recommends the local and hypodermic 
use of pituitary extracts (posterior lobe) . Obvious diseases of the nasal 
passages should be treated appropriately (see special treatises); and the 
general neurotic basis of the subject should be improved by the avoid- 
ance of mental and bodily overwork, and the use of iron, arsenic, 
phosphorus, strychnine, etc. 



DISEASES OF THE LARYNX. 



ACUTE CATARRHAL LARYNGITIS. 

Etiology. — Acute catarrhal laryngitis may occur at any age, but it 
is most common in adolescents and adults, especially in those debili- 
tated from any cause. The exciting causes are infectious, toxic, 
mechanical, or thermic irritants. The infectious form of the disease 
may be primary or secondary. Most primary cases are related eti- 
ologically to exposure, or "catching cold," and they are provoked 
by streptococci, staphylococci, pneumococci, influenza bacilli, Micro- 
coccus catarrhalis, etc. Secondarily, the disease may follow disease 
of the nose, throat, or bronchi, or it may occur as a manifestation or 
complication of certain infectious diseases (measles, scarlatina, influenza, 
typhoid fever, diphtheria, syphilis, tuberculosis, etc.). The toxic 
factors comprise the inhalation of irritant vapors (acids and alkalies); 
the excessive and prolonged use of tobacco, alcohol, etc.; gout, and 



518 DISEASES OF THE LARYNX 

sometimes the use of drugs, such as mercury, the iodides, etc. The 
mechanical factors comprise traumatism, inhalation of dust, the action 
of foreign bodies, overuse of the voice, etc. The thermal factors com- 
prise the action of very hot liquids, steam, etc. 

Pathology. — The lesions consist of swelling and redness of the mucous 
membrane, especially in the aryepiglottidean folds. The mobility of 
the vocal cords is impaired; sometimes there is considerable oedema; 
and there is more or less mucous or mucopurulent secretion. Occasion- 
ally there are minute submucous hemorrhages, and rarely superficial 
erosion of the mucous membrane (catarrhal ulcers), especially on the 
cords, the anterior commissure, or the interarytenoid fold. Inspissation 
of the secretion gives rise to a condition called laryngitis sicca. 

Symptoms . — At first there is a sensation of soreness or irritation and 
tickling or burning in the throat, a harsh, dry, sometimes spasmodic 
cough, and more or less alteration of the voice that may amount to 
complete aphonia. Phonation, deglutition, and inspiration (especially 
of cold air) are painful; dyspnea may be marked, especially in children, 
in whom it may be spasmodic and quite urgent (oedema). Expectora- 
tion at first is slight, but it soon becomes more abundant and mucous, 
or mucopurulent, occasionally blood-streaked. The general phenomena 
are usually slight — moderate fever for several days, headache, and 
malaise. Occasionally, especially in children and when the inflamma- 
tory phenomena are marked below the vocal cords, such narrowing of 
the lumen of the larynx may be produced that the symptoms resemble 
what have been ascribed to "croup" — crowing cough, stridor, and 
attacks of suffocation. These attacks often come on at night — due 
to accumulation of secretion and aspiration of the tongue. 

Diagnosis. — The diagnosis is usually easy, even without laryngo- 
scopy examination, which, however, may be required in doubtful 
cases. Laryngismus stridulus may be distinguished by the mode of 
onset, neurotic temperament, associated rickets, and the absence of fever, 
of coryza, of hoarseness, and of aphonia. Diphtheria may be dis- 
* tinguished by the more severe local and general symptoms, the presence 
of membrane on the tonsils or fauces, and early swelling of the cervical 
lymph nodes. Hysterical aphonia may be distinguished by the absence 
of fever and the results of the laryngoscopic examination. 

Prognosis. — The prognosis in adults is good, as a rule, the disorder 
ending in recovery in from three or four days to a week or more. In 
children a fatal termination may be induced by suffocation or a consecu- 
tive bronchitis or bronchopneumonia. 

Treatment. — Confinement of the room (the bed, in severe cases), 
rest to the larynx by the non-use of the voice, a mercurial purge, a 
diaphoretic febrifuge mixture (mentioned under coryza), and the in- 
halation of steam impregnated with menthol, compound tincture of 
benzoin, etc., suffice to bring about recovery in the majority of cases. 
Cold moist applications to the neck are often grateful to the patient. 
If the cough is very irritating, the throat may be sprayed with menthol, 



(EDEMATOUS LARYNGITIS 519 

cocaine, etc., or a Dover's powder or other sedative may be administered 
at night. The severe nocturnal attacks common in children are usually 
promptly relieved by an emetic and hot compresses to the neck. 



(EDEMATOUS LARYNGITIS. 

{(Edema of the Larynx; (Edema of the Glottis; Phlegmonous Laryngitis.) 

Etiology. — (Edematous laryngitis is peculiarly a disease of adult life, 
being uncommon in childhood. It may be primary or secondary. As a 
primary disorder it may be due to: (1) Infectious agents — whence it 
occurs (a) during the course of certain infectious diseases (smallpox, 
measles, scarlatina, typhoid fever, diphtheria, tuberculosis, syphilis, 
etc.); (b) as a concomitant of acute catarrhal laryngitis, laryngeal peri- 
chondritis, etc.; and (c) as an extension of the inflammatory oedema of 
Ludwig's angina, parotitis, tonsillitis, etc. (2) Toxic agents — inhalation 
of irritant vapors, the medicinal or other use of mercury, the iodides, 
etc. (3) Mechanical agents — foreign bodies impacted in the larynx. 
(4) Thermal agents — inhalation of steam. (5) Angioneurotic factors — 
angioneurotic oedema. As a secondary disorder it may occur (1) as a 
complication of general oedema (in heart disease, kidney disease, and 
lung disease), and (2) in consequence of pressure on the jugular veins 
(as by aneurysm of the aorta, tumors of the thyroid, mediastinum, etc.). 

Pathology. — The lesions consist of an inflammatory oedema, involving 
especially the aryepiglottic ligaments, the epiglottis, and the false vocal 
cords. The swelling is sometimes unilateral, sometimes subglottic, and 
may be so extreme as entirely to close the glottis. The mucous mem- 
brane is swollen, pale, grayish, and semitranslucent, or dull reddish in 
color. Rarely the exudation is purulent. 

Symptoms. — The symptoms are those of severe laryngitis, together 
with urgent dyspnoea — at first inspiratory and later expiratory stridor, 
inspiratory depression of the intercostal spaces, scorbiculus cordis, 
etc. Suffocation, that may lead almost immediately to a fatal issue, 
may be the first manifestation of the disease. The oedema is quite 
apparent on laryngoscopic examination; the swelling of the epiglottis 
may be detected by the finger or seen when the tongue is depressed. 

Diagnosis. — The diagnosis is easy from the symptoms and the results 
of laryngoscopic examination or palpation by the finger. 

Prognosis. — The prognosis depends upon the basic condition and 
the promptness with which treatment is instituted. The disease is 
often fatal. 

Treatment. — The patient should be given ice to suck, an ice collar 
should be applied externally, the throat and larynx should be sprayed 
with cocaine and adrenalin chloride, and the swollen areas should be 
scarified. If the symptoms are urgent, tracheotomy should be performed 
immediately, since the high mortality is due to delay. 



520 DISEASES OF THE LARYNX 

SPASMODIC LARYNGITIS. 

{Laryngismus Stridulus; Stridulous Laryngitis; Spasmodic Croup; False Croup.) 

Etiology. — Spasm of the larynx occurs in association with divers dis- 
eases of the larynx, but it is a dominant feature of the disorder known as 
spasmodic laryngitis or laryngismus stridulus. Probably these are dis- 
tinct disorders, the one an acute catarrhal laryngitis with spasm, the other 
a pure neurosis. The disorder is peculiar to children, especially rickety 
children, between the ages of six months and six years, and is said to be 
more common in boys. It is closely related to tetany, and may be one 
of its manifestations. In some cases it is related to enlargement of 
the thymus and receives the name thymic asthma (page 403). The 
attacks are often provoked by passion or emotional disturbances — 
so-called "passion fits" and "attacks of holding the breath." Whether 
the exciting cause acts centrally, as is supposed in rickets, or peripherally, 
has not been determined. Among the causes believed to act reflexly are 
adenoids, teething, indigestion, preputial irritation, intestinal parasites, etc. 

Pathology. — The lesions consist of paroxysmal tonic spasms of the 
adductor muscles of the glottis, in consequence of which the glottis 
is closed and breathing rendered impossible. There may or may not 
be an associated catarrhal laryngitis. 

Symptoms. — The attacks usually come on at night, the child having 
gone to bed well and being awakened out of a sound sleep. As a rule, 
there are no premonitory symptoms, no cough, no hoarseness. The 
attack begins with a forced inspiration, followed by complete cessation 
of respiration. The face, at first pale, becomes cyanotic and anxious, 
the eyes protrude and are rolled about, violent inspiratory efforts are 
made, the intercostal spaces and the abdomen become retracted, and 
profuse perspiration breaks out. The attack may last for from several 
seconds to several minutes, when suddenly with relaxation of the con- 
tracted adductors, a deep labored, noisy inspiration ("child-crowing") 
occurs, the cyanosis and anxious expression disappear, and the child 
becomes comfortable. In some cases there is loss of consciousness 
and tonic and clonic spasms of the trunk and extremities (carpopedal 
spasms). Rarely the attack leads immediately to death. Attacks 
vary much in severity, and they may occur singly or be frequently 
repeated — during the day as well as at night. 

Diagnosis. — The diagnosis is quite apparent from the symptomatology 
and the etiological factors. Membranous, or diphtheritic, laryngitis 
(true croup) may be distinguished by the presence of fever, the gradual 
development of the dyspnoea, and presence of a false membrane in the 
fauces or in the larynx on laryngoscopic examination. 

Prognosis. — The prognosis is good, since despite its alarming aspects, 
the disease is rarely fatal. 

Treatment. — During the paroxysm cold water should be dashed in 
the child's face, or the child should be placed in a warm bath (100° to 



CHRONIC LARYNGITIS 521 

105°) and cold water applied to its back and chest. Recourse may 
be had to a few whiffs of chloroform, or an emetic, such as ipecac. 
Recurrence of the attacks may be obviated by cold or counterirritation 
to the neck, and the internal use of bromides, chloral, belladonna, etc. 
All possible sources of peripheral irritation must be corrected. Since 
the children are anemic and rachitic, tonics containing iron, arsenic, 
phosphorus, strychnine, cod-liver oil, etc., and nutritious diet must be 
given for a long time. 



CHRONIC LARYNGITIS. 

(Chronic Laryngeal Catarrh; Preacher's Sore Throat.) 

Etiology. — Chronic laryngitis results from repeated attacks of acute 
laryngitis; the long continued and ill use of the voice (public speakers, 
preachers, singers, etc.); the continued action of injurious agents upon 
the larynx, such as tobacco smoke, dust (stone cutters, etc.), alcohol 
(inebriates), etc. 

Pathology. — The lesions, as a rule, consist of swelling, thickening, 
and pale grayish or bluish-red discoloration of the mucous membrane, 
especially of the epiglottis, the interarytenoid folds, and about the 
vocal cords. Rarely superficial erosions or ulcerations occur. Special 
types of the disease are described: Laryngitis hypertrophica, or ver- 
rucosa — verrucous projections or swellings the result of hyperplasia 
of the epithelium and the papillae; laryngitis atrophica- — pallor and 
thinness of the mucous membrane the consequence of atrophy; and 
laryngitis hypoglottica chronica hypertrophica, or chorditis vocalis 
inferior chronica — hyperplasia of the subchordal mucous membrane, 
leading to marked constriction of the laryngeal lumen. 

Symptoms. — The symptoms consist of irritation in the throat, cough, 
hoarseness, and expectoration — varying in severity from time to time. 
The sense of irritation compels the patient continually to attempt to 
clear the throat; the cough is rough, harsh; the hoarseness varies in 
degree to complete aphonia; and the expectoration is usually scanty, 
occasionally rather abundant, mucous, mocopurulent, and rarely 
blood-streaked. 

Diagnosis. — The diagnosis is usually quite obvious from the symptoms, 
but recourse should be had to laryngoscopic examination to ascertain 
the exact conditions, and to exclude tuberculosis, syphilis, tumors, etc. 

Prognosis. — The prognosis as to complete recovery is poor, but 
marked amelioration of the symptoms is possible. Relapses are com- 
mon, especially since the etiological factors are not readily controlled. 

Treatment. — Of prime importance is removal of the etiological 
factor — overuse of the voice, alcohol, tobacco, as the case may be. 
Change of climate — a sea voyage, residence in a pine forest, etc. — 
is often of the greatest benefit. Disease of the nose and throat 
must be corrected. Cold compresses externally are often of service. 



522 DISEASES OF THE LARYNX 

Approved internal remedies comprise the following, which may be 
applied on a swab or by means of an atomizer: Tannic acid (1 to 2 
per cent.), zinc sulphate (2 to 5 per cent.), potassium chlorate (2 to 5 
per cent.), silver nitrate (1 to 2 per cent.), alum (0.5 to 1 per cent.), 
etc. Insufflation of powders, bismuth, etc., is sometimes of service, 
if done carefully. The general health often demands the administration 
of tonics. 

LARYNGEAL PERICHONDRITIS. 

Etiology. — Laryngeal perichondritis may be rarely primary — when it 
is usually due to trauma; commonly it is secondary and occurs during 
the course of syphilis, tuberculosis, typhoid fever, diphtheria, scarlatina, 
erysipelas, etc. 

Pathology. — The cricoid and the arytenoid cartilages are most fre- 
quently affected; less commonly the thyroid and the epiglottis. Rarely 
the lesions are metastatic. Commonly there is at first more or less 
superficial ulceration of the mucous membrane — whence the lesions 
spread to the perichondrium. Usually the process goes on to abscess 
formation which gradually separates the perichondrium from the under- 
lying cartilage; soon the cartilage becomes necrotic and separates into 
small particles which with the other contents of the abscess are dis- 
charged — internally (perichondritis interna) or externally (perichondritis 
externa). The defect is usually remedied by cicatrization and conse- 
quent stenosis; but when the abscess is discharged externally a fistula 
not uncommonly results. 

Symptomatology. — Occasionally, especially in the primary affection, 
there may be an acute invasion, with chill (or chilliness) and fever. 
The characteristic symptoms consist of severe spontaneous pain, tender- 
ness on pressure over the larynx, hoarseness, cough, painful dysphagia 
(especially when the posterior portion of the cricoid cartilage is involved), 
and the development of laryngeal stenosis which may reach an extreme 
and dangerous degree. Laryngoscopic examination reveals redness 
and swelling of the mucous membrane, in some cases considerable 
oedema or a smooth localized swelling corresponding to the abscess. 
One or both vocal cords may become immobilized. In external peri- 
chondritis the swelling may be quite obvious and palpable; fluctuation 
may be obtainable; and the pus may gravitate to the mediastinum. 
Chronic laryngeal stenosis due to cicatricial contraction is a common 
event in the subjects that recover. 

Diagnosis. — The difficulty of making a satisfactory laryngoscopic 
examination often makes the diagnosis obscure; expectoration of a bit 
of cartilage often makes it conclusive. Tuberculosis, syphilis (gummas), 
and tumors, and in the external form, softened lymph nodes, must be 
excluded. 

Prognosis. — Death may occur from rapidly developing stenosis or 
the rupture of an abscess into the larynx. In subjects that recover, 



TUMORS OF THE LARYNX 523 

stenosis of the larynx and some impairment of the voice are 
common. 

Treatment. — In the acute stage, if stenosis is not marked, attempts 
may be made to reduce the swelling by the external use of an ice collar 
or leeches, and the internal use of hot drinks or hot inhalations, astrin- 
gents, or scarification of the mucous membrane. Tracheotomy or laryn- 
gotomy is often necessary, although the abscess may sometimes be 
opened internally, with favorable results. The patient's general health 
must be maintained by careful feeding and stimulants. In tuberculous 
and syphilitic cases the general disease should be treated. In chronic 
stenosis dilatation may prove useful, or the patient may be obliged to 
wear a tracheal cannula. 



TUMORS OF THE LARYNX. 

Pathology. — Tumors of the larynx may be benign or malignant. 
The benign tumors occur at all ages, but are most common in adult 
life, and in males rather than in females. They comprise: papilloma 
(pinkish or grayish wartlike, sessile or pedunculated growths, often 
multiple); fibroma (spheroidal, smooth, firm, dense growth, usually 
single); mucous polyp, soft fibroma, myxofibroma (soft, translucent 
growth); chondroma (firm, hard, smooth); lipoma (rare, soft, yellow- 
ish); angioma (reddish, hemorrhagic); and cysts (small, transparent, 
fluctuating growths, usually retention cysts). Papilloma and fibroma 
are the most common, especially in children. Benign growths usu- 
ally spring from the vocal cords, except the mucous polyp and cysts 
which are often found in the ventricles of Morgagni and on the epiglottis. 
The malignant tumors comprise sarcoma and carcinoma. Sarcoma 
is rare; occurs, as a rule, early in life; and forms soft or hard, smooth 
or diffuse infiltrations, sometimes verrucose growths, that commonly 
spring from the vocal cords. Carcinoma is more common; occurs, 
as a rule, in middle life or later; and forms wart-like excrescences, 
diffuse infiltrations, or soft, nodular, rapidly ulcerating growths, that 
involve the vocal cords, the ventricles of Morgagni, or the epiglottis. 
Sometimes the carcinoma is secondary to carcinoma of the tongue, 
pharynx, or oesophagus. 

Symptomatology. — Of benign tumors, the most common symptoms 
are alterations in the voice (harsh, croaking, aphonia); cough (some- 
times croupy in children); dyspnoea, varying in grade, depending upon 
the size and situation of the growth, and sometimes paroxysmal when the 
growth is pedunculated and mobile; orthopncea, sometimes progressing 
to asphyxiation, from sudden occlusion of the glottis; and dysphagia, 
when the upper surface of the epiglottis is involved. Pain is often 
inconspicuous. 

Of malignant tumors, the symptoms are quite like the foregoing. 
In some cases the voice is not affected — when the posterior surface of 



524 DISEASES OF THE TRACHEA AND THE BRONCHI 

the cricoid cartilage, the epiglottis, or the aryteno-epiglottidean fold 
alone is involved. Hoarseness, when it does develop, may be due to 
the growth itself, or to immobility of the vocal cords. When the epi- 
glottis or the posterior surface of the larynx is involved, dysphagia is 
usually marked, and there may be increased salivation, a fetid secretion 
(sometimes blood-streaked, from ulceration), and an offensive breath. 
Pain radiating to the ear or the temporal region may be present. The 
cervical lymph nodes may become enlarged from metastases. Cachexia 
develops when the growth has become extensive, or when it is primary 
elsewhere. 

Diagnosis. — Tumors of the larynx are to be diagnosticated only by 
laryngoscopic examination. Decision as to malignancy frequently 
depends upon removal of a portion of the growth and its study histologi- 
cally. Benign tumors, as a rule, are pedunculated, multiple, do not 
infiltrate, show little tendency to bleed or ulcerate, and do not recur 
after removal. Rapid growth and recurrence after removal are signifi- 
cant of malignancy. Malignant tumors may be distinguished from 
syphilis and tuberculosis by the age of the patient, definite tumor forma- 
tion, its primary localization to one side, the early immobility of the vocal 
cords, early ulceration, tendency to bleeding, pain, glandular involve- 
ment, the absence of tubercle bacilli in the secretions, and the non- 
response to antisyphilitic treatment. 

Prognosis. — The prognosis in benign tumors is good, both with 
reference to life and the preservation of the voice. In malignant tumors 
the prognosis, as a rule, is bad, although in some cases the growth may 
be removed by early operative procedures. 

Treatment. — The treatment of tumors of the larynx is surgical. Most 
benign tumors may be removed by intralaryngeal methods under local 
anesthesia. In children this is difficult, and thyrotomy, subhyoid 
pharyngotomy, or laryngotomy may be necessary. In malignant 
tumors partial or complete laryngectomy offers the only hope of success. 
When metastasis has occurred laryngectomy is usually useless; the 
patient may be made comfortable by tracheotomy and the subsequent 
use of a tracheal cannula. 



DISEASES OF THE TKACHEA AND THE BRONCHI. 



ACUTE BRONCHITIS. 

(Acute Bronchial Catarrh; Acute Tracheitis; Acute Tracheobronchitis.) 

Etiology. — Acute bronchitis may occur at any age, but it is prob- 
ably most common during adolescence and adult life, although it is 
more serious and fatal in the very young and the very old. It is 
more common in males than in females, on account of their mode 



ACUTE BRONCHITIS 525 

of life and occupations. It prevails especially during changeable (moist 
and cold) weather — the late fall, the winter, and the early spring. 
Sedentary life, working in close, ill-ventilated rooms, debility from any 
cause predispose to the disease; an out-of-door life is a preventive. 
It may occur as a primary, independent affection, or in association 
with (or secondary to) other disorders. The exciting causes of the 
primary disease are the infectious, toxic, mechanical, and thermic irri- 
tants provocative of acute catarrhal laryngitis (page 517); indeed, the 
one often follows the other, and both result from "catching cold." 
Divers bacteria appear to be the most common cause. As a second- 
ary disease, it occurs in many infections, such as measles, scarlatina, 
pertussis, diphtheria, influenza, typhoid fever, malaria, syphilis, tuber- 
culosis, etc.; it is common in the subjects of chronic heart disease, 
chronic lung disease, Bright's disease, gout, etc. Some persons seem 
unusually susceptible (hereditary influences?). 

Pathology. — The mucous membrane of the trachea and bronchi 
is red, swollen, and covered with mucus and mucopus; occasionally 
there may be punctiform hemorrhages. The lesions may extend to 
the finer bronchi — and collapse, bronchopneumonia, emphysema, or 
oedema and congestion of the lungs may result. The microscopic 
lesions consist of inflammatory hyperemia of the mucosa, oedema and 
cellular infiltration of the submucosa, and swelling and desquamation 
of the lining epithelial cells. 

Symptomatology. — Depending upon the extent and intensity of the 
manifestations, three forms of acute bronchitis may be distinguished: 
(1) A mild form, in which the lesions are confined to the trachea and 
the main bronchi; (2) a more severe and more diffuse form, in which 
the medium-sized and the smaller bronchi also are involved; and (3) 
a form in which the finest bronchi and bronchioles are involved — 
capillary bronchitis (identical with bronchopneumonia). In rare cases, 
the onset is abrupt, and attended by a chill; chilliness is not uncom- 
mon. In many cases an acute coryza precedes the bronchitic phenom- 
ena; laryngeal symptoms also may be associated. 

In the mild form the symptoms consist of substernal distress, pain, 
or a sense of rawness or oppression, and cough, at first hard, harsh, 
often paroxysmal and painful, especially beneath the sternum and 
along the attachment of the diaphragm. In the beginning there may 
be no expectoration, or with considerable effort a small amount of 
tough, viscid, occasionally blood-streaked mucus may be expelled; 
after a few days, however, the sputum becomes more abundant, less 
viscid, and mucous or mucopurulent, in character. There may be 
little or no general disturbance, though commonly there is some languor 
and headache, possibly, but not always, some elevation of the tempera- 
ture. In the more severe forms, the general and the local symptoms 
are aggravated. Languor, weariness, and headache are usually more 
marked; general neuromuscular pains are often quite severe; and the 
temperature may be 102° F., or thereabouts, for at least a day or two. 



526 DISEASES OF THE TRACHEA AND THE BRONCHI 

The cough may be extremely distressing, but, as in the milder form, it 
becomes much ameliorated with the development of free expectora- 
tion. There may be some dyspnoea and acceleration of the pulse rate. 
Cyanosis, not uncommon in the young and the aged, suggests capillary 
bronchitis (bronchopneumonia). 

Physical Signs. — In the mild form, when the lesions are confined to 
the trachea and the main bronchi, there may be no abnormal physical 
signs, aside from harshness of the breath sounds and some prolongation 
of the expiration. In the more severe form, in addition to the foregoing, 
sonorous and sibilant rales may be heard, especially at the bases pos- 
teriorly, in the early stages, and fine and coarse bubbling rales later 
when the bronchial secretion has become freer. In children there are 
often evidences of interference with free ventilation of the lungs — dysp- 
noea, inspiratory retraction of the lower end of the sternum and the 
lower ribs, use of the accessory muscles of respiration, etc. 

Diagnosis. — The diagnosis, as a rule, is easy. The bilateral distribu- 
tion of the physical signs is important. One should not overlook the 
fact that bronchitis may be the initial manifestation of certain infectious 
diseases, such as measles, pertussis, typhoid fever, malaria, etc. A 
history of exposure to any of these infections is valuable. The sputum 
should be examined to determine the nature of the infecting agent. 
Persistence of fever for more than several days suggests something 
more than mere bronchitis. Capillary bronchitis (bronchopneumonia) 
is indicated by severe general symptoms, fever, dyspnoea, and cyanosis. 
Croupous pneumonia should be readily differentiated by the absence 
of the characteristic physical signs. Predominance of fine rales at 
the apices, rather than at the bases, suggests tuberculosis — even in 
chronic bronchitic subjects. The diagnosis of the secondary form of 
bronchitis presupposes the recognition of the primary cardiac, pulmon- 
ary, renal disease, etc. 

Prognosis. — Except at the extremes of life, a fatal termination is 
rare. Mild cases usually subside within a week, and convalescence 
is established at the end of two weeks. In severe cases the course is 
more protracted. One attack often predisposes to another. In the 
very young and the aged, in emphysematous, cardiac, and nephritic 
subjects, the disease is commonly serious and may lead to a fatal termina- 
tion. 

Treatment. — Although not always possible, it is desirable that the 
patient go to bed for a day or two; at least, he should remain at rest 
in a well-ventilated room, and his diet should be restricted. The 
attack may sometimes be aborted by Dover's powder (10 grains, 0.6 
gram), hot lemonade (with or without whiskey), and a hot mustard foot- 
bath at bed time, followed in the morning by calomel or blue mass and 
a saline laxative in adults, or castor oil in children. A mustard plaster, 
or turpentine stupe applied to the chest serves to relieve the local tight- 
ness and soreness; or the chest may be rubbed with camphorated oil or 
camphor liniment. 



CHRONIC BRONCHITIS 527 

In the early stages much relief is afforded by a sedative diaphoretic 
mixture, such as the following: 

1$ — Spirit of nitrous ether 3 drams 12J00 

Wine of ipecac V/2 drams 6 00 

Potassium citrate 3 drams 12 00 

Cinnamon water, sufficient to make .... 3 ounces 100 00 — M. 

S. — Two teaspoonfuls (10 c.c.) every three hours (to an adult). 

If the pulse is very rapid or there is much fever, minim doses of tincture 
of aconite may be added to each dose (especially serviceable in children). 
Additional relief to the dryness of the throat and the difficulty in breath- 
ing is afforded by inhalations of steam impregnated with sodium chloride, 
sodium bicarbonate, compound tincture of benzoin, etc.; or the Dover's 
powder may be repeated at night, or codeine or heroin substituted, but 
discretion must be exercised in the use of these, remedies in the young 
and the aged. 

If, after several days, the cough continues troublesome and the 
expectoration has not become free, the following old-fashioned mixture 
will be found efficacious: 



1$ — Ammonium chloride ......... 1}4 drams 6 

Syrup of squill 3 drams 12 

Compound mixture of glycyrrhiza .... 3 ounces 100 

S. — Two teaspoonfuls (10 c.c.) four times daily. 



00 
00 
00— M. 



Paroxysms of coughing (referable to bronchial spasm) may be controlled 
by belladonna, stramonium, or lobelia; belladonna is efficacious also if 
the expectoration is copious and continues for a long time — in which 
event the balsamic preparations also are useful — such as terebene, ter- 
pene hydrate, tar, etc. In children, if the expectoration is abundant 
and not well raised (provoking dyspnoea and cyanosis) an emetic should 
be administered — alum (20 grains, 1.3 gram) or wine of ipecac (1 dram, 
4 c.c, repeated in ten minutes, if necessary). Signs of prostration and a 
weak heart call for the administration of stimulants. During convales- 
cence, nutritious diet, fresh air, and tonics, stomachics, quinine, strych- 
nine, iron, and arsenic, should be given. 



CHRONIC BRONCHITIS. 

(Chronic Bronchial Catarrh; Chronic Catarrhal Bronchitis ; Winter Cough.) 

Etiology. — Chronic bronchitis is rare as a primary disorder; but it 
may occur as a result of repeated acute attacks, or it may be chronic 
from the outset in consequence of the continued inhalation of irritating- 
dust, vapors, etc. It is not uncommon in the middle aged and the 
aged, recurring each year with the cold, damp, and changeable fall and 
winter weather. Often it is secondary to chronic cardiac, pulmonary, 
or renal disease. It is also a manifestation of gout. 



528 DISEASES OF THE TRACHEA AND THE BRONCHI 

Pathology. — The condition of the bronchial mucous membrane 
varies in different cases. Often it is thickened irregularly, hyperemic, 
and covered with mucopus; in places the epithelium may be entirely 
wanting — granular patches. The fibrous and muscular coats are 
usually thickened and the seat of cellular exudation. In long-con- 
tinued cases more or less atrophy occurs, and leads to cylindrical dilata- 
tion (bronchiectasis) or diverticula. Emphysema, fibroid induration 
of the lung, and hypertrophy of the heart (especially of the right ven- 
tricle) are common concomitants. 

Symptomatology. — The principal symptoms are cough, expectoration, 
and dyspnoea — which vary much in different cases, and permit of the 
differentiation of several types of the disease. 

Chronic Winter Cough. — This is probably the most common variety, 
and is characterized by the recurrence each winter of cough, which 
usually is not very troublesome, and expectoration, moderate in amount, 
mucous or mucopurulent in character. These usually lessen or dis- 
appear during the late spring, the summer, and the early autumn. 

Chronic Bronchitis with Emphysema.— -This is very common, and 
usually results from repeated attacks of acute bronchitis or of recurrent 
attacks of winter cough. The cough is often troublesome; it is more 
marked in the morning (accumulation of secretion during the night), 
and may be violent or paroxysmal; it commonly lessens or disappears 
during the summer. The expectoration may be scanty, viscid, and diffi- 
cult to raise; or it may be abundant, and mucopurulent or seropurulent 
in character; occasionally nummular. Substernal distress, and more 
or less dyspnoea (especially after coughing or exertion) are common. 
The general health is often maintained for years. 

Dry Chronic Catarrh (Catarrh Sec) of Laennec. — This is characterized 
by a dry, troublesome, paroxysmal cough, dyspnoea, tightness of the 
chest and very scanty expectoration, which often contains grayish, 
pearl-like particles that are raised with difficulty. Emphysema is often 
associated; asthmatic attacks occur from time to time; and the subjects 
are prone to attacks of acute bronchitis. 

Gouty bronchitis is an obstinate form, sometimes associated with 
other manifestations of gout. Dyspnoea is often extreme. Marked 
pulmonary congestion may lead to the expectoration of blood-stained 
sputum. There is usually associated disease of the heart, liver, and 
kidneys. 

Fetid (or putrid) bronchitis, although usually seen in association 
with gangrene or abscess of the lung, bronchiectasis, the decomposition 
of the contents of tuberculous cavities, the rupture of an empyema or 
subdiaphragmatic abscess into the lung, etc., sometimes occurs as an 
independent affection. The cough is usually paroxysmal and severe; 
the sputum is usually abundant (upward of a pint in twenty-four hours), 
malodorous, thin, seropurulent in character, and on standing separates 
into three layers — the lowermost consisting of purulent material, detritus, 
and irregular masses the size of peas (Dittrich's plugs) ; a middle layer 



CHRONIC BRONCHITIS 529 

of discolored fluid; and an upper layer of frothy mucus. Fever, 
loss of appetite, and other manifestations of bacterial intoxication are 
not uncommon. Should the disorder be primary, secondary changes, 
such as gangrene or abscess of the lung, septic metastases (as in the 
brain, etc.), may occur. 

Bronchorrhoea may follow long continued bronchitis of the ordinary 
type. The cough and expectoration often occur in paroxysms, and 
are associated with extreme dyspnoea. The expectoration is very 
abundant— as much as one or two quarts in the twenty-four hours; 
it is usually thin, frothy, serous or mucoserous, occasionally some- 
what purulent or hemorrhagic, rarely thick and distinctly purulent, 
in character. The condition may lead to permanent dilatation of the 
bronchi, and fetid bronchitis. In the young especially it often persists 
for a long time without noteworthy impairment of the general health. 

Physical Signs. — The physical signs commonly include those of em- 
physema. In the absence of emphysema the percussion note is reso- 
nant, as a rule; there may be some impairment, especially posteriorly, 
in the event of there being much secretion, collapse of small areas of 
the lung, thickening of the pleura, etc. The breath sounds are usu- 
ally harsh and vesicular in character, the expiration prolonged; and 
there are rales, sibilant and sonorous, or fine and coarse bubbling, or 
crackling, especially posteriorly, depending upon the conditions within 
the bronchi. In the dry catarrh no rales are present. Evidences of 
hypertrophy and dilatation of the right ventricle may also be detected. 

Diagnosis. — As a rule, the diagnosis is easy. Care must be exercised 
to exclude pulmonary tuberculosis (repeated examination of the sputum, 
etc.), and one must remember that a chronic bronchitic subject may 
become tuberculous. Distinction must be drawn between the primary 
cases and those due to chronic cardiac, pulmonary, and renal con- 
ditions. Aortic aneurysm, mediastinal and pulmonary tumors, etc., 
have been mistaken; but the physical signs, if sought for, are usually 
conclusive. 

Prognosis. — Chronic bronchitis, as a rule, is a very obstinate disease, 
tends to recur, and to become worse with advancing years ; but recovery 
is not impossible, and marked amelioration of the symptoms is readily 
attained. The prognosis is good in young subjects, and in older sub- 
jects able to live in a suitable climate. The prognosis is bad in 
subjects of chronic heart, pulmonary, and renal disease, and in the aged. 

Treatment. — Removal to a warm, moist, equable climate (Florida, 
Southern California, Riviera, etc.) constitutes the most successful 
treatment — prophylactic as well as curative. Those unable to avail 
themselves of this should keep their room warm, though well ventilated, 
live outdoors as much as possible in sunny, pleasant weather, avoid 
vitiated atmospheres; in a word, avoid the factors known to provoke 
a "cold." The diet should be nutritious and easily assimilable. In 
patients the subject of chronic cardiac, pulmonary, or renal disease, gout, 
etc., the primary disorder must receive careful and appropriate treat- 
34 



530 DISEASES OF THE TRACHEA AND THE BRONCHI 

ment. Thus, some patients are much improved by small doses of 
digitalis, strophanthus, convallaria, and other heart tonics; attention 
to free elimination by the kidneys and free evacuation by the bowels 
materially improve others; whereas, the obese and the gouty often 
respond markedly to a proper dietetic regimen. Attention to the 
general health, and the use of cod-liver oil, arsenic, iron, quinine, and 
strychnine are followed by good results in other cases. 

Medicinal treatment directed to the bronchitic condition must be 
varied to suit the exigencies of each individual case. In some cases 
the treatment need not be different from that appropriate in the later 
stages of acute bronchitis. Often potassium (or ammonium or sodium) 
iodide is of marked benefit, especially when the cough is paroxysmal 
and associated with emphysema; often it may serviceably be com- 
bined with ammonium chloride (or carbonate) and lobelia; or if secre- 
tion is free, with squill or senega; but the use of the iodide should not 
be too long continued. In most cases the balsamic preparations are 
of much value — oil of sandalwood, of eucalyptus, of turpentine, and 
of copaiba; balsam of Peru or of tolu; terpene hydrate, terebene, tar, 
creosote, etc. I have seen much benefit from 30 minims (2 c.c.) each of 
syrup of tar and syrup of wild cherry, four times a day. If the cough is 
distressing at night, resort must often be had to opium or its deriva- 
tives, codein, heroin. The troublesome morning cough may sometimes 
be relieved by the use of alkalies (sodium chloride, sodium bicarbonate, 
potassium acetate, etc.) in hot water. The dry distressing cough may 
be benefited by inhalations of steam impregnated with sodium chloride, 
tincture of benzoin, oil of eucalyptus, white pine, etc. In fetid bronchitis 
the odor may be improved by sprays of carbolic acid (0.05 to 0.1 per cent.), 
thymol (0.2 to 0.5 per cent.), or by resort to intratracheal medication. 
Severe dyspnoea and pain in the chest may be relieved by local applica- 
tions to the chest, such as plasters, dry or wet cups, hot or cold com- 
presses, etc., or by venesection. Methodic compression of the thorax 
during expiration, the use of the pneumatic cabinet, and posture that 
favors the exit of secretion are of service in some cases. 



FIBRINOUS BRONCHITIS. 

Etiology. — Fibrinous bronchitis, a disease attended by the formation 
of so-called fibrinous casts of the bronchi, may be primary or secondary. 
The primary is an independent disorder, rare, and of obscure etiology. 
It occurs about middle life, twice as frequently in men as in women, 
prevails during the winter and spring, and tends to recur from year to 
year. It may affect persons previously well or the subjects of bronchitis 
or tuberculosis. The secondary form has been observed in certain infec- 
tious diseases, such as diphtheria, scarlatina, measles, pneumonia, influ- 
enza, typhoid fever, etc.; in certain chronic cardiac and pulmonary 
diseases; in diseases of the skin, such as pemphigus, herpes, impetigo, 



FIBRINOUS BRONCHITIS 531 

etc.; complicating menstruation and pregnancy; etc. Casts of the 
bronchi have also been seen in association with the albuminous expec- 
toration that sometimes follows tapping a pleural effusion; and blood 
casts occur with hemoptysis. These secondary forms are not at present 
under consideration. 

Pathology. — The characteristic lesion consists of the formation of 
membranous, partly hollow, partly solid, casts of the bronchi, which, 
dividing dichotomously, may reach to the finest bronchi. The sub- 
jacent mucous membrane may appear intact, or its epithelium may be 
shed and it may show the usual evidences of chronic bronchitis. The 
lesions are often curiously confined to definite areas, which in the recur- 
ring form are sometimes repeatedly and only involved. The casts are 
grayish white in color, occasionally covered with streaks of blood, 
and vary much in size from small irregular pieces to masses measuring 
six to eight inches in length. On transverse section they present a 
concentric appearance. Usually said to be fibrinous, recent investiga- 
tions seem to show that they are made up mostly of mucin; some 
observers believe them to consist of syntonin or coagulated albumin. 
Microscopically the ground substance contains leukocytes (mostly 
mononuclear), epithelium, sometimes erythrocytes, Charcot-Leyden 
crystals, and Curschmann's spirals. Various microorganisms have 
been cultivated from the membrane, especially pneumococci, strepto- 
cocci, and staphylococci. The nature of the process is ill understood, 
but it is sometimes considered analogous to mucous colitis. The rare 
disorder known as acute obliterating fibrinous bronchiolitis is doubtless 
of like nature. 

Symptomatology. — Acute and chronic forms of the disease may be 
distinguished. The acute form is rare, and usually begins suddenly 
with a chill (or chilliness), fever, cough, expectoration, and dyspnoea. 
At first and for several days, as a rule, the attack resembles an ordinary 
bronchitis; soon, however, the cough becomes severe and paroxysmal; 
the expectoration, which heretofore has been mucous in character, is 
raised with considerable difficulty; dyspnoea becomes urgent, and 
eventually with a more or less violent effort the characteristic cast is 
expelled — with great relief to the patient. The expectoration again 
becomes more abundant and may contain small coagula. There is 
sometimes associated hemoptysis; rarely a large hemorrhage. The 
attack may last several days or several weeks. 

The chronic form may develop out of a chronic bronchitis or tubercu- 
losis, and between attacks there are usually the ordinary evidences 
of bronchitis. The attacks are less severe than in the acute form, 
and they recur at longer intervals, often yearly; there is usually little 
or no fever, and the dyspnoea is less urgent. Should the attacks recur 
at short intervals, small coagula are likely to be expectorated frequently 
and the general health of the patient may deteriorate. 

Physical Signs. — The physical signs are those of bronchitis. Over 
the portion of lung affected there may be weakened or absent breath 



532 DISEASES OF THE TRACHEA AND THE BRONCHI 

sounds, and fine bubbling rales may be provoked by voluntary coughing. 
After the loosening of the cast, before its expectoration, a rough clicking 
sound (bruit de drapeau, Ventilgerausch) is said to be audible. 
I Diagnosis. — The diagnosis depends upon the detection and recogni- 
tion of the casts. These may be small and escape observation. Their 
detection is facilitated by floating them on water. Severe paroxysms 
of coughing and dyspnoea relieved by expectoration are suggestive, and 
should lead one to search for the casts. Care must be taken to exclude 
the secondary form of the disease. 

Prognosis. — The prognosis in acute cases is grave, death occurring 
in from one-third to one-half the cases from suffocation or broncho- 
pneumonia. The chronic variety may last for many years, but eventu- 
ally recovery may ensue. Tuberculosis, emphysema, atelectasis, pleu- 
ritis, and chronic heart disease are rather common sequels. 

Treatment. — In the acute cases, the treatment is that of acute bron- 
chitis; and the only hope of cure in the chronic cases is the cure of 
the commonly associated chronic bronchitis. Inhalations of atomized 
sodium carbonate or bicarbonate (2 to 5 per cent.), lime water, or com- 
pound tincture of benzoin, mitigate the distress and are said to assist 
in loosening the membrane. Pilocarpin, since it promotes free bron- 
chial secretion, is useful for the same purpose. Potassium iodide is 
probably of even more value. Mercurial inunctions also have been 
recommended. In the event of marked dyspnoea, cyanosis, and delayed 
expectoration, emetics should be resorted to. 



BRONCHIECTASIS. 

Etiology. — Bronchiectasis, dilatation of the bronchi, may be due to 
a congenital defect — in which event it is likely to be universal; other- 
wise, it results from weakening of the bronchial wall, which, in con- 
sequence, becomes unable properly to withstand the distending force 
of the contained air (much exaggerated during paroxysms of coughing). 
Acland has well classified the causes, as follows: (1) In the lumen 
of the bronchial tubes, (a) the impaction of a foreign body, and (b) 
the inhalation of fibrinous plugs, as in diphtheria; (2) (a) acute 
affections of the walls of the bronchial tubes, resulting from pneu- 
monia, bronchopneumonia, tuberculosis, diphtheria, and whooping 
cough, and (b) chronic affections of the wall of the bronchial tubes, 
such as chronic bronchitis (60 per cent, of the cases), syphilitic peri- 
bronchial fibrosis with stenosis, and tuberculosis; (3) affections of the 
parenchyma of the lung, such as chronic interstitial pneumonia (10 
per cent, of the cases), and collapse from causes other than pressure; 
(4) affections external to the lung, such as aneurysm, neoplasm, and 
pleural adhesions and thickening (12.5 per cent, of the cases). The 
disease is more common in males than in females. About 50 per cent, 
of the cases occur between the twentieth and the fortieth year; 23 per 



BRONCHIECTASIS 533 

cent, between the tenth and the twentieth year; and 13 per cent, 
between the fortieth and the fiftieth year. 

Pathology. — The bronchiectatic cavities may be cylindrical, fusiform, 
saccular, or moniliform, but the cylindrical and the saccular are the 
more common, and may exist together. The condition may be general — 
in which event it is unilateral, rarely congenital, and commonly follows 
pneumonia; or it may be partial — in which event it is bilateral and 
occurs in tuberculosis (especially at the apex), pleurisy (especially at 
the base), and emphysema. In the general form the entire bronchial 
tree consists of a series of sacculi communicating the one with the other, 
lined with a smooth, glistening mucous membrane (frequently transition 
of cylindrical epithelium into flat), except in the dependent portions 
where there may be some ulceration; the dilatations are sometimes 
extreme, forming large cysts that may extend to the pleural surface; 
the intervening pulmonary tissue is indurated and fibrotic. In the 
partial form, the mucous membrane is inflamed and ulcerated and 
the muscular tissue thin and atrophic; cicatrization may give rise to 
stenosis of the lumen. The contents of the cavities are often horribly 
fetid, and on culture reveal divers pyogenic microorganisms, the 
influenza bacillus, etc. 

Symptomatology. — Most of the symptoms are those of the chronic 
bronchitis, emphysema, tuberculosis, etc., with which the bronchi- 
ectasis is associated; in many of these cases the existence of the bronchi- 
ectasis is not even suspected. The characteristic symptoms consist 
of: (1) Cough, which, from time to time, especially in the morning or 
the evening, or on sudden change of posture, becomes exaggerated 
into violent paroxysms, and results in the expulsion of (2) usually a 
large amount (500 c.c. or more) of grayish, acid, fetid, mucopurulent 
sputum, which on standing separates into three layers — the lowermost, 
dense, purulent, and granular; the middle, watery and sometimes 
discolored; and the uppermost, frothy, discolored, and mucous. Micro- 
scopically, it consists of mucus, pus, detritus, fatty acid and hema- 
toidin crystals, elastic fibers (when ulceration has occurred), bacteria, 
etc. Sometimes it contains a notable amount of blood; sometimes 
large hemorrhages occur. (3) Fetor of the breath, especially on coughing 
(it may be missed if the cavities are in the apex and well drained). 
(4) The physical signs of cavity formation. The temperature is 
variable; it may be normal even when the sputum is fetid; but in 
the event of necrosis of the bronchial wall and toxic absorption, it 
corresponds to' the septic type. Dyspnoea and cyanosis on exertion are 
common. 

An acute and fatal form of the disease is not uncommon in children 
(bronchiolectasis), and is usually associated with bronchopneumonia. 

Complications and Sequels. — Complications and sequels are many. 
Pneumonia, abscess and gangrene of the lung, interstitial pneumonitis, 
empyema, pyopneumothorax, etc., are common; septicemia, pyemia, 
metastatic abscesses (brain, liver, kidney), clubbing of the finger tips, 



534 DISEASES OF THE TRACHEA AND THE BRONCHI 

hypertrophic pulmonary osteo-arthropathy, amyloidosis, etc., are not 
uncommon. 

Diagnosis. — In the absence of the characteristic symptoms the disease 
often escapes clinical recognition. Tuberculous cavities, as a rule, are 
more common at the apex, preceded by signs of solidification, progressive 
in character, and the expectoration contains tubercle bacilli; whereas, 
bronchiectatic cavities are more common at the base, followed by indu- 
ration of the lung, often non-progressive, and the expectoration does 
not contain tubercle bacilli; but tuberculosis may supervene upon non- 
tuberculous bronchiectasis. Fetid sputum with normal temperature is 
almost certainly from a bronchiectatic cavity. 

Prognosis. — Cure is extremely unlikely, if it occurs at all; but the 
patient may live for many years and lead a fairly active life. Death 
usually results from septicemia, emaciation, or one of the complications 
or sequels. The acute form is usually fatal from asphyxia. 

Treatment. — Attention to the primary disorder and the general health 
of the patient are of prime importance. The best medicinal treatment 
consists of the inhalation of vaporized creosote, for fifteen minutes every 
other day at first, later every day. A dram or two of crude creosote 
should be poured on some water contained in a saucer and slowly vapor- 
ized over an alcohol lamp. This often at first provokes coughing, which 
has the effect of ridding the bronchial tubes of retained secretion and 
then permitting the local action of the creosote on the mucous mem- 
brane. Inhalations of carbolic acid, eucalyptus, menthol, etc., are 
of much less value. Intratracheal injections are sometimes of service; 
Grainger Stewart's is one of the best: Menthol, 10, guaiacol, 2, and 
olive oil, 88, of which two to three drams (8 to 12 c. c.) should be injected 
at a time. There is much more likelihood of good effect if the injection 
follows soon upon a copious expectoration — cleansing of the bronchi. 
The internal use of balsamic preparations, oil of sandalwood, terebene, 
terpene hydrate, etc., should be tried. The adoption of postures that 
favor drainage of the cavities is of value. Surgical drainage has been 
practised in some cases with good results. 



BRONCHIAL ASTHMA. 

(Spasmodic Asthma.) 

Bronchial asthma is a disorder characterized by attacks of dyspnoea 
(chiefly expiratory) and a characteristic expectoration; it commonly 
occurs in bronchitic subjects, and ultimately leads to emphysema. 

Etiology. — Asthma is not infrequently familial; it is twice as common 
in men as in women; it may occur at any age; and it sometimes develops 
during childhood and persists throughout life. The attacks are excited 
by divers stimuli — emotion, fright, unpleasant odors, irritating dust, 
certain articles of diet, too much food (overloaded stomach), cold and 
damp atmosphere, etc. Some subjects are freer while in the country, 



BRONCHIAL ASTHMA 535 

others while in the city. The disorder has much in common with hay- 
fever, and both may occur at the one time or alternate in the same 
subject. 

Pathology. — The nature of the disorder is not well understood. In 
many cases it seems to be chiefly, if not wholly, a neurosis, and due 
to spasm of the bronchial muscles or swelling of the bronchial mucous 
membrane, in consequence of disorder innervation — pneumogastric 
or vasomotor. Others attribute the phenomena to spasm of the dia- 
phragm, of all the inspiratory muscles, or of the musculature of the 
pulmonary arteries. In many cases, however, and this is especially 
important, although frequently overlooked, there is inflammation of 
the bronchioles (bronchiolitis exudativa of Curschmann), attended 
by swelling of the mucosa, the exudation of a viscid mucus, and 
desquamation of the surface epithelium — which assuredly suffice to 
explain the phenomena. In some cases there is associated disease of 
the nose (hypertrophic rhinitis, polyps, adenoids), of the larynx and 
trachea (catarrh, enlarged bronchial lymph nodes), disease of the geni- 
talia, etc., which often apparently stand in causal relationship to the 
asthma. Most subjects reveal the lesions of chronic bronchitis; others 
are gouty, nephritic, etc. 

Symptomatology. — The essential' symptoms consist of attacks of 
dyspnoea followed by the expectoration of a characteristic sputum. 
Though usually not, the attacks are sometimes preceded by premonitory 
symptoms (a sense of constriction or oppression of the chest, flatulence, 
etc.), aura asthmatica. They commonly come on during the night, 
the patient being awakened from a sound sleep by dyspnoea and a 
sense of suffocation that soon become extreme and often induce him 
to seek an open window in the hope of relief. The chest soon becomes 
fixed in full expansion, the accessory muscles of respiration become 
tense and make violent, though useless, efforts, and the expiration 
becomes much prolonged, labored, and accompanied by loud wheezing. 
The respirations, as a rule, are not much increased in frequency; the 
pulse is small and accelerated, the temperature is usually normal or 
subnormal, the extremities become cool, the face livid, the expression 
anxious, and sweat not infrequently breaks out. 

Early in the attack there is usually little or no cough or expectoration. 
After several hours, however, sputum begins to be expectorated; this 
consists of a small amount of viscid mucus containing roundish gela- 
tinous masses (perles of Laennec) which represent casts of the bronchioles 
(bronchiolitis); many of these have a twisted spiral arrangement 
(Curschmann's spirals), and may or may not reveal a central translucent 
filament. In addition, the sputum contains leukocytes (mostly eosino- 
philic), epithelium from the bronchi and the alveoli, and Charcot- 
Leyden octahedral crystals. Examination of the blood usually reveals 
an eosinophilia (25 to 50 per cent.). 

A single attack may last from upward of a half hour to several hours, 
or the patient for days, sometimes for several weeks, may partially 



536 DISEASES OF THE TRACHEA AND THE BRONCHI 

recover and relapse, especially at night. At the end of several days 
in severe attacks, sooner in milder attacks, the sputum becomes more 
abundant, mucopurulent in character, and Curscbmann's spirals 
disappear. At this time the patient's general distress becomes much 
lessened, although he is likely to remain weakened, apathetic, and 
dyspnceic for some time; indeed, more or less dyspnoea is not uncommon. 
The patient may remain free from attacks of asthma for weeks, months, 
or years at a time. 

Physical Signs.— During the asthmatic attack the chest is usually 
in full inspiratory expansion and fixed; inspiration is short and jerky, 
the movements of the chest are altogether disproportionate to the efforts 
of the accessory muscles of respiration; the diaphragm is depressed 
and almost immobile; the percussion note is normal or hyperresonant 
(especially in long-standing cases in which emphysema develops); 
on auscultation the expiration is prolonged, and there are sibilant and 
sonorous rales. Later the rales become crackling or fine or coarse 
bubbling. 

Diagnosis. — The diagnosis is usually easy; the symptoms, the char- 
acteristic sputum, and the physical signs distinguish asthma from other 
disorders attended by dyspnoea. Uremic asthma is differentiated by 
the signs of nephritis, high tension pulse, albuminuria, hypertrophy 
of the left ventricle (hypertrophy of the right ventricle occurs in long- 
standing asthma). Cardiac asthma, hysterical asthma, hay fever, 
spasm of the glottis, etc., sometimes must be considered the differential 
diagnosis. 

Prognosis. — The prognosis is fairly good in early life, especially if 
a local cause (adenoids, nasal polyps, etc.) can be found and remedied. 
Recovery can scarcely be expected in middle and advanced life when 
chronic bronchitis, emphysema, hypertrophy and dilatation of the 
heart, etc., have developed, but the patient's suffering may be much 
ameliorated and he may live to a ripe old age. Although the individual 
attacks appear to be extremely severe, death during an attack is very 
rare. 

Treatment. — Careful attention must be given to all the circumstances 
of the patient's life. Some do much better in the city, despite its smoke, 
and dirt, and soot, than in the purer atmosphere of the country; but 
climatic treatment must be instituted with reference to the response 
of each individual patient. The diet must be carefully regulated: 
the gouty and the obese must be abstemious; and in all cases, par- 
ticularly in those disposed to flatulency, it is wise to advise the heavy 
meal in the middle of the day, and the partaking of very little food 
toward evening. The bowels should be opened at least once daily. 
Sleeping in a room the atmosphere of which is laden with steam (im- 
pregnated or not with the vapor of oil of eucalyptus, oil of pine, etc.) 
or with the fumes of burning nitre may secure freedom from nocturnal 
attacks and a consequent peaceful sleep. All sources of local irrita- 
tion (nasal, pharyngeal, etc.) must be remedied. 



TRACHEAL AND BRONCHIAL OBSTRUCTION 537 

During the attack relief may be obtained by the inhalation of amyl 
nitrite or chloroform, or the fumes evolved by burning the leaves 
(cigarettes) of belladonna, stramonium, lobelia, hyoscyamus, tobacco, 
or by burning paper impregnated with potassium nitrate; by drinking 
hot coffee and whiskey or spirit of chloroform; or by the hypodermic 
use of morphine (combined with atropine or cocaine), or pilocarpine — 
to be employed with caution. Tincture of lobelia in dose sufficient to 
produce the physiological effect is often efficacious, but it should not 
be employed when the heart is weak. An emetic sometimes assists 
in expelling retained secretions. An imminent attack may sometimes 
be warded off, or aborted, by the prompt use of amyl nitrite, nitro- 
glycerin (-J--Q grain, 0.0013 gram, hypodermicly), or chloroform. 

Between the attacks no drug is so useful as potassium (or sodium) 
iodide; it has rendered me the best service when combined with 
lobelia. From time to time one of the bromides also may be added. 
Nitroglycerin is quite useful in some cases, especially in those with 
high arterial tension. Adrenalin chloride (hypodermicly), euphorbia 
pilulifera, arsenic, the compressed air of the pneumatic cabinet, oxygen, 
etc., appear to have been useful in some cases. When the heart is 
weak strophantus or digitalis, in small doses, is serviceable. 



TRACHEAL AND BRONCHIAL OBSTRUCTION. 

Etiology. — Obstruction of the trachea or the bronchi may be due to : 
(1) A foreign body in the lumen; (2) stenosis the result of disease of 
the wall; and (3) compression from without. 

Foreign bodies, depending upon their size, may cause partial or com- 
plete obstruction. Usually the obstruction is incomplete and bronchia 1 
rather than tracheal. The foreign body commonly passes throug] 
the trachea and is arrested in a bronchus, the right usually, since i 
is larger and more in a direct line with the trachea than the left. 

Stenosis due to disease of the tracheal or bronchial wall may I: 
caused by syphilis (usually), tuberculosis, leprosy, polyps, carcinoma, 
sarcoma, ecchondroma, etc. When due to syphilis, the stenosis m?^ 
be annular, but it is also often somewhat longitudinal. The new 
growths may be situated anywhere, but they are more common in the 
bronchi near the bifurcation of the trachea. 

Compression of the trachea or bronchi from without may be caused 
by tumors and other enlargements of the thyroid or thymus; enlarge- 
ments of the regional lymph nodes (tuberculosis, leukemia, Hodgkin's 
disease, sarcoma, carcinoma), aneurysm, mediastinal abscess, Pott's 
disease or tumors of the vertebrae, etc. 

Symptomatology. — The symptoms vary with the site and degree of 
the obstruction. A foreign body of sufficient size may lodge suddenly 
in the trachea, and cause complete obstruction and immediate death 
from asphyxia. A small body in the trachea, such as a pin, may cause 



538 DISEASES OF THE TRACHEA AND THE BRONCHI 

only a local sense of discomfort and dyspnoea. Bodies of moderate 
size (which sometimes may be unconsciously aspirated) occasion sudden 
onset of coughing and dyspnoea, paroxysmal exacerbations of the cough- 
ing and dyspnoea (sometimes attributable to accumulation of secretions 
below the obstruction), inspiratory and expiratory stridor, and the 
common phenomena of defective ventilation of the lungs — inspiratory 
depression of the suprasternal fossa and of the scorbiculus cordis, 
depression of the intercostal spaces, pulsus paradoxus, etc. The larynx 
moves but little in contrast to the marked movement that obtains in 
laryngeal obstruction; laryngoscopic examination reveals no disorder 
of the larynx; bronchoscopic examination may reveal the cause of the 
symptoms. The factors causing compression of the trachea from 
without, being usually in the neck, are quite obvious to the senses. 

In bronchial obstruction, the signs and symptoms are usually uni- 
lateral, in contrast to the bilateral phenomena of tracheal obstruction. 
The respiratory movements of the affected side are limited, and may 
be completely absent if the obstruction is of high grade. If the obstruc- 
tion is of moderate grade, the breath sounds are harsh and broncho- 
vesicular in character and the fremitus is diminished; if of high grade, 
the breath sounds are much diminished or absent — which with normal 
percussion resonance is of much significance. A loud stenotic sound 
may be audible about the site of the obstruction. In most cases there 
is more or less dyspnoea — usually inspiratory. In long-standing cases 
some considerable difference in the circumference of the two sides may 
develop — due to inactivity of the affected side and compensatory emphy- 
sema of the other side. In some cases obstruction of one bronchus 
is followed by obstruction of the other bronchus or the trachea — as 
in mediastinal tumors, etc. A foreign body may lead to ulceration 
of the bronchial mucosa with consecutive bronchopneumonia or abscess 
or gangrene of the lung. Pressure from without, as by an aneurysm, may 
lead to retention of secretions with consecutive bronchiectasis, broncho- 
pneumonia, and abscess or gangrene of the lung, or to collapse of the lung. 

Diagnosis. — The diagnosis is usually easy. The site of bronchial 
obstruction may sometimes be determined by the area of diminished 
breath sounds, the point of maximum intensity of a stenotic murmur, 
by recourse to tracheoscopic or bronchoscopic examination, or, in the 
event of certain impervious foreign bodies, by recourse to the cr-rays. 

Prognosis. — The prognosis depends upon the cause of the obstruction. 
Foreign bodies, while they sometimes occasion sudden death, are also 
sometimes retained for months or years, and finally expectorated. 

Treatment. — The treatment depends upon the cause of the obstruction. 
Foreign bodies may sometimes be removed by inverting the patient 
and exciting coughing; by direct removal with the aid of the broncho- 
scope ; sometimes by recourse to tracheotomy or bronchotomy. Syphilis 
and tuberculosis are to be treated according to the basic condition. 
Tumors may be removed sometimes, but with much difficulty and little 
prospect of permanent good. 



HEMOPTYSIS 539 



DISEASES OF THE LUNGS. 

HEMOPTYSIS. 

(Pulmonary Hemorrhage; Bronchopulmonary Hemorrhage.) 

Etiology. — Hemoptysis, the spitting of blood or the discharge of 
blood from the respiratory tract, may result from disease of the 
larynx, the trachea, the bronchi (including the bronchioles), or the 
lung. The diseases of which it is a manifestation are: (1) Dis- 
eases of the respiratory system: (a) Diseases of the larynx — acute 
and chronic inflammation; tuberculous, syphilitic, and malignant 
ulceration, etc. Laryngeal hemorrhage is unusual; occasionally it 
is profuse, as in altered blood states, etc. (b) Diseases of the bronchi 
and trachea — bronchitis (especially the putrid and fibrinous varieties); 
bronchiectasis; tuberculous, syphilitic, and malignant ulceration (with 
erosion of a branch of the pulmonary artery); rupture of an aneurysm 
into the trachea or a bronchus, in which event the hemorrhage may 
be large and lead immediately to a fatal issue; etc. (c) Diseases of 
the lungs, especially tuberculosis (80 to 90 per cent.) of the cases, croup- 
ous pneumonia, the acute exanthemas, congestion, thrombosis, and 
embolism (infarction), abscess, gangrene, tumors, actinomycosis, 
aspergillosis, zooparasite infections, etc. In the early states of tuber- 
culosis the blood usually comes from the congested mucosa of small 
bronchi (capillary oozing); in the later stages it is due to erosion of 
an artery or the rupture of an aneurysmal dilatation of a branch of 
the pulmonary artery. (2) Diseases of the cardiovascular system: (a) 
Advanced valvular disease (especially mitral stenosis), leading to well- 
marked passive congestion. The hemorrhage may be slight and 
recurrent, or quite free, sometimes persisting for several days, (b} 
Aneurysm of the aorta, in which, at first, the hemorrhage may be smal 
and repeated, and due to pressure on the bronchial mucosa, or to leakag 
through the outer (usually fibrous) coat of the aneurysmal sac (so- 
called weeping of the aneurysm); or the hemorrhage may be very larg 
(rupture of the aneurysm) and lead speedily to death. (3) Disease^ 
of the blood — hemophilia, purpura, scurvy, leukemia, anemia, etc., 
and the disorganization of the blood that occurs in yellow fever, etc. 
(4) Diminished atmospheric pressure, as in mountain sickness, and too 
sudden release from caissons. (5) Arteriosclerosis and gout, so-called 
arthritic hemoptysis, sometimes observed in arteriosclerotic and gouty 
subjects with disease of the smaller vessels of the lungs. (6) Vicarious 
hemoptysis, sometimes observed in women at the time of menstruation 
or during the persistence of amenorrhcea. (7) Traumatism — injuries 
of the thorax, punctured wounds of the chest and lung, and rupture 
of a small vessel due to overexertion. (8) Neurotic hemoptysis, occa- 
sionally observed in neurotic, hysterical (especially female) subjects 



540 DISEASES OE THE LUNGS 

who otherwise are well. Some of these subjects remain perfectly well, 
but some subsequently become definitely tuberculous. 

Symptoms. — Rarely hemoptysis develops in persons previously in 
perfect health; thus, it may be the initial manifestation of tubercu'osis 
or of an aortic aneurysm. Usually, however, symptoms of the causative 
disease precede the hemoptysis (which itself is only a symptom). The 
blood lost varies in amount from the slightest streak in a previously 
mucous sputum to that sufficient immediately to cause death. When 
small in amount the hemoptysis itself may be the only noteworthy 
symptom; when profuse, it is often preceded by a sense of warmth 
or discomfort in the chest, or of tickling or of something arising in the 
throat, and a saline taste in the mouth — which are followed immediately 
by the ejection of the blood, bright red, fluid, and frothy. The blood 
may be coughed up, or it may escape from the patient's mouth without 
obvious effort on his part. Large hemorrhages are commonly associated 
with mental perturbation, cardiac palpitation, marked prostration, 
and often syncope; immediate death may ensue, but it is rare. Fatal 
hemorrhage may occur into a tuberculous or other cavity without the 
blood being discharged externally. In other cases some of the blood 
effused into a cavity or bronchus is retained some time and then dis- 
charged clotted; casts of the bronchi and bronchioles may be observed. 
Sometimes the blood is swallowed and later vomited; or it may escape 
into the intestine and discolor the stools. 

Physical Signs. — The physical signs, as a rule, are only those of the 
primary disease, with the later development of fine and coarse bubbling 
rales, due to the presence of blood in the bronchi and bronchioles. 

Diagnosis. — The diagnosis, as a rule, is quite easy. Hemorrhage 
from the nose, mouth, fauces, and pharynx must be excluded (usually 
obvious on local examination). In hematemesis the symptoms and 
signs point to disease of the abdominal viscera; sensations of warmth 
in the epigastrium, nausea, and of faintness often precede the discharge 
of blood — which is vomited; the blood is usually dark in color, clotted, 
acid in reaction, often mixed with food, and is quite likely to appear 
in the stools. 

Prognosis. — The prognosis depends upon the underlying disease 
and the amount of blood lost. Usually, the hemorrhage ceases spon- 
taneously; but occasionally death occurs — more commonly, however, 
after than during the bleeding. 

Treatment. — Absolute bodily and mental rest is essential. The 
patient should be reassured. If, as in tuberculosis, the diseased side 
is known, or if it is discoverable by the presence of rales anteriorly 
(the patient should not be disturbed for a physical examination) he 
may lie on the diseased side (to lessen the respiratory movements and 
to prevent aspiration of blood into the bronchi of the other lung). Ice 
may be given to the patient to suck, and an ice bag may be applied 
to the bleeding side, or to the precordium (to lessen cardiac excite- 
ment). Tranquillity may be favored by the hypodermic use of morphine 



CONGESTION OF THE LUNGS 541 

combined with atropine — which is also of value in restraining the cough ; 
morphine, however, should be used rather sparingly in large hemor- 
rhages, since by lessening the cough (benumbing sensibility), it may 
lead to inundation of the bronchial system with blood. Lowering 
of the blood pressure (the formation of a clot) should be favored by 
nitroglycerin, sometimes by aconite, veratrum viride, or chloroform, 
etc.; by purgation; by giving the minimum amount of food (cold, not 
hot) consistent with the patient's general condition; and by avoiding 
the use of cardiac stimulants, such as alcohol, strychnine, digitalis, 
strophanthus, caffeine, etc., even if syncope ensues. Syncope itself 
is a valuable adjunct in the formation of a clot. Sodium chloride on 
the tongue (reflex action on the vagus), and calcium chloride (30 grains, 
2 grams) may prove of service. Small repeated hemorrhages may 
sometimes be controlled by the continued use of turpentine, or aromatic 
sulphuric acid. Ergot, adrenalin chloride, etc., are to be avoided, 
since they raise the blood pressure. Gelatin, gallic acid, lead acetate, 
etc., are of at least doubtful value. The hypodermic injection of 
normal serum has been recommended, especially in recurring 
hemoptyses. 



CONGESTION OF THE LUNGS. 

{Hyperemia of the Lungs; Pulmonary Congestion.) 

Congestion of the lungs may be active or passive. 

Active Congestion. — Active congestion of the lungs usually occurs as 
a secondary, symptomatic affection, but it is said occasionally to occur 
as a primary, independent affection. Symptomatically it may be circum- 
scribed or diffuse, and involve one lung or both lungs. It is usually seen 
in association with other disorders of the lung, such as pneumonir 
pleurisy, bronchitis, embolism and thrombosis, tuberculosis, etc. J 
times it appears to be due to the inhalation of various toxic agenf 
such as hot air, irritating vapors, etc., to sudden changes from cold 
heat, great physical exertion, profound emotion, etc. In France it 
recognized as a common independent disease, and has received f 
name "maladie de Woillez." Most of these cases, however, are 
doubtless atypical pneumonias, of which one proof is the finding of 
pneumococci in the sputum (believed by some writers to be attenuated 
pneumococci). 

Symptoms. — The symptoms consist of cough, dyspnoea, and slight 
frothy, blood-streaked sputum, in addition to the symptoms of the 
associated disease. La maladie de Woillez is manifested by initial chill, 
fever (101° or more), cough, dyspnoea, and pain in the side of several 
days' duration. The physical signs are those of the first stage of pneu- 
monia — slight impairment of percussion resonance, feeble or broncho- 
vesicular breath sounds, increased fremitus, and fine crepitant rales. 

Treatment. — The treatment is that of pneumonia. 



542 DISEASES OF THE LUNGS 

Passive Congestion. — Two forms of passive congestion of the lungs 
are distinguished: (1) Mechanical, and (2) hypostatic. 

Mechanical congestion results from obstruction to the return flow 
of blood to the left heart. It is common, therefore, in chronic mitral 
valvular disease, dilatation of the right ventricle, etc.; and it occurs 
sometimes in consequence of the pressure of mediastinal tumors. The 
lungs are enlarged, tough, elastic, heavy, and of a reddish-brown color 
(cyanotic induration), which quickly changes to a bright red color on 
section and exposure to the air (oxidation of the hemoglobin). Micro- 
scopically there are dilatation of the interalveolar capillaries, over- 
growth of fibrous connective tissue, and in the walls of the alveoli, as 
well as free in the alveoli, many blood-pigmented cells (heart-disease 
cells of the sputum). 

Hypostatic congestion occurs in many acute febrile diseases (typhoid 
fever, etc.), in chronic debilitating diseases, anemic, marantic, and 
cachetic conditions, in coma (apoplexy, and other disorders of the 
brain, morphine and other narcotic poisonings), in old age, etc. 
It results from a feeble circulation, loss of tone of the pulmonary 
vessels, and the influence of gravity. Usually the condition is limited 
to the bases of both lungs posteriorly. The affected portions of the 
lungs are surcharged with blood, dark red in color, oedema tou's, and 
often entirely devoid of air, whence they sink in water (hypostatic 
pneumonia; splenization). Occasionally in organic disease of the brain 
(apoplexy, etc.), the condition may be unilateral; and it is sometimes 
associated with definite areas of bronchopneumonia (aspiration pneu- 
monia). 

Symptoms. — The symptoms are often equivocal. Usually, however, 
there are cough, frothy, blood-streaked expectoration (containing pig- 
mented, so-called heart-disease cells), dyspnoea, and more or less cya- 
nosis. Physical examination reveals impaired percussion resonance 
posteriorly at the bases, increased fremitus, feeble or bronchovesicular 
breathing, and fine and coarse bubbling rales. 

Diagnosis. — The diagnosis depends more upon the presence of a 
causative factor and the results of the physical examination than upon 
the symptoms. 

Prognosis. — The prognosis depends upon the causative factor; usually 
amelioration of the symptoms may be brought about. 

Treatment. — The underlying cause of the condition, usually organic 
disease of the heart, must be treated. If the symptoms are urgent, 
venesection should be performed; those who accept great hazards some- 
times suggest tapping the right auricle — a procedure that does not 
appeal to me. Diffusible stimulants are often of much temporary 
value. The hypostatic form of the disease may often be prevented 
by having susceptible patients frequently turned in bed, or placed in 
a semiprone or upright position in bed or in a chair from time to time. 






(EDEMA OF THE LUNGS 543 



(EDEMA OF THE LUNGS. 

(Acute and Chronic Pulmonary (Edema; Recurrent Pulmonary (Edema; Acute 
Suffocative Pulmonary (Edema.) 

Etiology. — Pulmonary oedema, the transudation into the alveoli and 
the interstitial tissue of the lungs, of a serous, sometimes serosanguino- 
lent, fluid, occurs under divers circumstances: (1) As an agonal mani- 
festation in many acute and chronic disorders, especially of the heart 
and bloodvessels, kidneys, lungs, blood, nervous system (brain), etc.; 
(2) as an acute transitory manifestation in disease of the heart, kidneys, 
and in certain infectious diseases; (3) as a chronic process in disease 
of the heart, and under circumstances akin to those that produce 
chronic, or passive, congestion; (4) after thoracentesis; (5) associated 
with inflammatory processes in the lung, especially pneumonia, tubercu- 
losis, thrombosis, embolism, etc. (so-called inflammatory or collateral 
oedema; not a true oedema — rather an exudation); (6) as an apparently 
primary, acute, often quickly fatal disorder, developing without obvious 
exciting cause (acute suffocative pulmonary oedema). 

The mechanism of the oedema varies in different cases. Often, as 
maintained by Welch, it is "due to a disproportion between the working 
power of the left ventricle of such a character that, the resistance 
remaining the same, the left heart is unable to expel in a unit of time 
the same quantity of blood as the right heart. Such disproportion may 
be brought about by paralysis or by spasm of the left ventricle," and 
increasing the pressure in the pulmonary circulation it leads to transu- 
dation of serum through the pulmonary capillaries. Disturbances of 
the innervation of the cardiopulmonary plexus by periaortitis, consider- 
able augmentation of the vascular tension in the small circulation, 
and acute or rapid insufficiency of the right ventricle (Huchard), serve 
to explain the cases associated with angina pectoris, Hodgson's diseas 
and other diseases of the aorta. The toxic vasomotor theory (paralys 
of the pulmonary vessels) serves to explain the cases occurring in Bright 
disease, in pregnancy (without valvular or other heart disease); \hi 
associated with angioneurosis; and that due to certain drugs, such i 
the iodides, pilocarpine, etc. Congestion by recoil (Riesman) explains 
those cases developing after thoracentesis, the oedema in these cases 
resulting from an afflux of blood to the expanding lung and a leakage 
of serum through the pulmonary vessels, which by reason of long com- 
pression have become changed and rendered more permeable. In- 
creased fluidity of the blood is perhaps a factor in some cases. 

Pathology. — The oedema may be limited to the bases, or it may be 
gene al and involve both lungs. The cedematous lung is bulky, pale, 
boggy; contains less air than normally (but does not sink in water); 
and on section a clear, frothy, serous or serosanguinolent fluid, of low 
specific gravity and containing a trace of albumin, exudes, especially 
on pressure. 



544 DISEASES OF THE LUNGS 

Symptoms. — In addition to the symptoms of the primary disease, 
dyspnoea, cough, and expectoration are the noteworthy manifestations. 
The expectoration is especially characteristic, being usually abundant, 
thin, serous (occasionally serosanguinolent), and frothy. The dyspnoea 
sometimes becomes much aggravated and amounts to orthopncea, the 
accessory muscles of respiration being called into activity. As a rule, 
there is more or less cyanosis; the pulse becomes small, rapid, and of 
poor tension, and the extremities become cold. There is no fever, unless 
bronchopneumonia or other infectious complication ensues. 

Acute suffocative pulmonary cedema apparently is an independent 
disorder that develops suddenly, often without obvious exciting cause, 
and frequently leads quickly to a fatal termination, although recurring 
attacks are by no means uncommon. It occurs, as a rule, in arterio- 
sclerotic, cardiac, and nephritic subjects, and is characterized by the 
sudden development, often at night, of attacks of extreme dyspnoea 
(orthopncea), cyanosis (pallid lividity), cough, expectoration of a thin, 
frothy, serous, albuminous (occasionally blood-streaked) fluid, and 
marked prostration (with sweating, etc.). The fluid often drools from 
the patient's mouth without effort on his part; I have seen twelve 
ounces of such fluid expelled within a few hours. The attack may 
result in death within ten or fifteen minutes, the patient being virtually 
drowned in his own fluids ; or it may subside rather soon (within a half 
hour or thereabout), or it may last from three to twelve or more hours. 
The condition of the heart varies during the attacks; in one patient 
that I observed the right heart seemed to be considerably dilated during 
the attack. 

Physical Signs. — Physical signs consist of general impairment of the 
percussion resonance, or scattered foci of dulness and intervening areas 
of vesiculotympanitic sound (relaxation of the lung tissue), feeble, 
harsh, or obscured vesicular breathing, and numerous fine and coarse 
bubbling rales (localized or distributed generally throughout both lungs). 

Diagnosis. — The diagnosis is easy; the symptoms and physical signs 
can scarcely be mistaken for anything else. An associated broncho- 
pneumonia should not be overlooked. 

Prognosis.— The prognosis is grave, especially in view of the asso- 
ciated phenomena, of which the oedema is often a terminal manifestation. 

Treatment. — The treatment, as a rule, is that of the disease of which 
the cedema is one manifestation. A hypodermic injection of morphine 
(J grain, 0.015 gram) and atropine (y^o" grain, 0.0006 gram) will 
usually almost immediately relieve the severe symptoms; I have seen 
it render the greatest service (apparently save life) in the acute suffo- 
cative type of the disease. The injection may be repeated, if the cir- 
cumstances demand it; repeated injections of atropine are often of 
value for a day or two. In addition, diffusible stimulants are indi- 
cated — camphor, strychnine, ether, whiskey, etc., hypodermicly; stro- 
phanthus, coffee, brandy, whiskey, champagne, etc., by the mouth. 
Venesection is sometimes a life-saving procedure, and should be resorted 



PULMONARY EMBOLISM AND THROMBOSIS 545 

to when the patient's condition is grave (extreme cyanosis, etc.). 
Counterirritation (dry or wet cups, mustard poultices, etc.) may prove 
of service. Drastic purgatives are often given in the hope of relieving 
the system of fluid, but their action is too severe to recommend their 
use while the patient is seriously ill. Nor does the use of emetics to 
assist in the expulsion of the fluid commend itself to me. Since the 
disorder is often a terminal manifestation, treatment in these cases may 
not prove of avail. 



PULMONARY EMBOLISM AND THROMBOSIS. 

{Pulmonary Infarction; Hemorrhagic Infarction of the Lung; Pulmonary Apoplexy.) 

Etiology. — Primary thrombosis of the pulmonary artery or its branches 
is an unusual event, but it may result from slowing of the circulation, 
impoverishment of the blood, and disease of the arterial wall, such as 
may occur in pneumonia (and other infections), arteriosclerosis, com- 
pression of the vesse by a tumor, etc. Pulmonary embolism results 
from thrombotic processes in the right side of the heart or in the systemic 
veins, especially the femoral veins, the veins of the uterus (after par- 
turition), the sinuses of the brain, the veins of the abdomen, liver, etc. 
It is common in the sequence of mitral valve disease, especially stenosis, 
in which passive congestion of the lungs and dilatation of the right 
side of the heart have supervened, the thrombi developing in the auricle 
or amidst the columnar carnese. The foundation of the embolus may 
also be a newgrowth that has invaded a vein, a phlebolith, fat set free 
by a fracture of a long bone, rupture of the liver, rupture of the sub- 
cutaneous adipose tissue, air bubbles, etc. The embolus, as well as the 
thrombus, may be infectious or non-infectious. 

Pathology. — The embolus or thrombus may involve the main branch 
of the pulmonary artery, one or several of the medium-sized branches, 
or the smallest branches. The blocking of the vessel is usually, but 
not always, followed by infarction; sometimes not, because death occurs 
almost immediately; in other cases, because the obstruction is not 
complete, or the collateral circulation is sufficient, or the bronchial 
arteries maintain the circulation. Stasis of the pulmonary circulation 
seems to be an important if not essential element in the process of 
infarction. The infarct may be single, though they are usually multiple; 
they are more common in the lower lobe on the right side; they vary 
in size from a marble to an orange; they consist of pyramidal or wedge- 
shaped masses, with the base toward the periphery, dark red in color, 
firm, and devoid of air. Microscopicly they are found to consist of 
blood filling the air vesicles and infiltrating the lung tissue. The 
thrombus or embolus often escapes detection. The overlying pleura 
is often covered with a fibrinous exudation, through which small foci 
of hemorrhage may be observed. Small infarcts may be absorbed, 
or the blood may be removed by reestablishment of the circulation; 
35 



546 DISEASES OF THE LUNGS 

large infarcts leave behind a puckered scar. Should the embolus be 
infective, pneumonia, abscess or gangrene of the lung, pleuritis or 
pyopneumothorax, etc., may result. 

Symptoms. — Complete obstruction of a main branch of the pulmonary 
artery is often followed by immediate death; in other cases, after a 
few moments of a feeling of extreme constriction within the chest, 
dyspnoea, and terror, the patient loses consciousness, the pupils dilate, 
the face becomes livid, the pulse rapid and irregular, perspiration 
breaks out, and death occurs within an hour. In less severe cases, 
that is, in cases in which the obstruction is not complete or the obstructed 
vessel is small, the chief symptoms consist of sudden pain and a sense 
of constriction within the chest, dyspnoea (labored, sometimes Cheyne- 
Stokes breathing), hemoptysis, and more or less collapse. Bloody, 
dark-red, non-aerated expectoration is quite significant of infarction. 
A typical ll stitch in the side" sometimes ensues, and is referable to a 
concomitant pleurisy; it is usually associated with local tenderness 
and a friction rub. Fever does not occur, unless the embolus is infective; 
in this event, to the general manifestations of septicopyemia are added 
the local signs of pulmonary abscess or gangrene. Occasionally small 
infarcts develop without noteworthy symptoms. 

Physical Signs. — There are no characteristic physical signs. Small 
peripheral and central infarcts usually occasion no physical signs what- 
ever; but larger infarcts that reach the pleura may occasion dulness 
on percussion, harsh bronchial or bronchovesicular breath sounds, 
and crepitant or crackling rales. Should there be a local pleuritis, 
the breath sounds may be feeble or inaudible, and frictions may 
develop. 

Diagnosis. — The diagnosis may be exceedingly easy, as in a chronic 
heart subject in whom the symptoms develop typically; in other cases, 
it may be quite difficult — in case of sudden death. In these cases, 
the diagnosis is facilitated by the presence of a causative factor, and 
the absence of definite causes for thrombosis or embolism of the coronary 
artery, cerebral hemorrhage, rupture of an aneurysm, and other causes 
of sudden death. 

Prognosis. — The prognosis, as a rule, is unfavorable. If death does 
not occur soon, the infarction, nevertheless, points to weakness of the 
right ventricle, a primary thrombus somewhere in the body, or other 
serious disorder. Occasionally the infarct is absorbed and the patient 
recovers temporarily, at least. Recurrences are rather common. 

Treatment. — Prophylaxis is of the utmost importance. Patients in 
whom venous thrombi exist, or who are ill with diseases known to favor 
the development of such thrombi, should be carefully nursed, protected 
from sudden movements that might dislodge the thrombus, and well 
fed. At the time of the development of the embolism, morphine and 
atropine are usually necessary to relieve pain; if the patient does not 
die soon, recourse should be had to stimulants — camphor, strychnine, 
ammonia, oxygen, etc. Later the primary disorder requires attention. 



ATELECTASIS AND COLLAPSE OF THE LUNG 547 

ATELECTASIS AND COLLAPSE OF THE LUNG. 

(Apneumatosis ; Compression of the Lung.) 

Atelectasis and collapse of the lung are much-related conditions: 
atelectasis properly is a condition found in infants in which the lungs 
or portions of the lungs have not expanded; collapse occurs in older 
persons and is a reversion to this condition after expansion has occurred. 
Both terms, however, are commonly used interchangeably. Congenital 
and acquired forms of the condition are usually distinguished. 

Etiology. — Congenital atelectasis results from inefficient action of 
the respiratory muscles (associated usually with general feebleness 
of the infant); defective innervation resulting from a congenital defect 
or from pressure on the foetal head by the forceps or a contracted pelvis ; 
obstruction of a bronchus by mucus or meconium, or by pressure 
from without, as by enlarged lymph nodes; or by pressure on the 
lung by enlarged abdominal organs, tympanites, ascites, etc. 

Acquired atelectasis, or collapse, of the lung results from: (1) 
Obstruction of a bronchus by mucopus, foreign bodies, newgrowths, 
or c^her products of inflammation. It is found most commonly in asso- 
ciation with bronchopneumonia. When the obstruction is complete, 
air can neither enter nor leave the involved portion of the lung, and 
absorption of the air by the blood takes place. (2) Compression of a 
bronchus by a pleural effusion, hydrothorax, pneumothorax, pyothorax, 
pericardial effusion, extreme cardiac hypertrophy, aneurysm of the 
arch of the aorta, newgrowths of the thorax and mediastinum, kypho- 
scoliosis, and pressure from below the diaphragm by enlarged viscera, 
tympanites, ascites, etc. (3) Feeble respiratory efforts, such as occur 
in debilitated and asthenic conditions generally — cachectic and maran- 
tic states, typhoid fever, coma, prolonged dorsal decubitus, paralysis 
of the pneumogastric nerves, rachitis, pleural adhesions, kyphoscoliosis, 
etc. 

Pathology. — Atelectasis most commonly involves the lower portions 
of the lungs; it may occur in scattered foci (obstruction within the 
bronchi,) or it may implicate an entire lobe (compression from without). 
The collapsed portion of the lung is reduced in size, purplish red in 
color, firm, airless, and sinks in water; sometimes there is serous infil- 
tration (splenization, carnification). In the congenital variety the 
atelectatic portions of the lung may gradually expand, or they may 
remain unexpanded and become the seat of fibrous thickening — hypo- 
plasia or aplasia of the lung. The condition is often associated with 
congenital anomalies of the circulation (patulous ductus Botalli, fora- 
men ovale, etc.). 

Symptoms. — Congenital atelectasis is manifested by feeble and super- 
ficial respiration, dyspnoea, cyanosis, cold extremities, feeble heart 
action, drowsiness, sometimes muscular twitchings and convulsions 
(carbon dioxide poisoning). The physical signs consist of deficient 



548 DISEASES OF THE LUNGS 

expansion of the chest, retraction of the intercostal spaces, and defective 
inspiratory murmur over the atelectatic portions of the lung. 

The symptoms of acquired atelectasis are often obscured by those 
of the primary disorder, commonly bronchopneumonia, and the collapse 
often is not diagnosticated. In other cases, dyspnoea, cyanosis, feeble 
heart action, cold extremities, etc., develop, but it is difficult to say 
whether these are not due as much to the primary disorder as to a 
supposed collapse of the lung. In cases associated with kypho- 
scoliosis, cyanosis, dyspnoea, and palpitation of the heart are usually 
marked, and in consequence of the obstruction in the pulmonary circu- 
lation considerable hypertrophy and dilatation of the right ventricle 
ensue; ultimately lack of compensation supervenes. 

Physical Signs. — When associated with bronchopneumonia there 
are often no noteworthy physical signs in addition to those occasioned 
by the bronchopneumonia; sometimes to the evidences of localized 
foci of solidification are added those of intervening (or surrounding) 
foci of inflation. When the collapsed area is large (compression of 
a bronchus from without), there is restricted movement at the base of 
the chest (or over the collapsed area), with increased expansion 
elsewhere, impaired percussion resonance, diminished fremitus, and 
feeble breath sounds; occasionally, when the air has access to the main 
bronchus, there may be increased fremitus and bronchovesicular breath- 
ing. Crackling rales are not uncommon; frequently they disappear 
after repeated deep inspirations. 

Diagnosis. — The disorder is often overlooked when the foci are small; 
when large, the physical signs serve for their recognition. Changes 
in the dulness, breath sounds, and rales after several deep breaths 
or a change of posture (for several hours) serve to exclude many 
other disorders, such as pneumonia, pleuritis, thrombosis and em- 
bolism, etc. 

Prognosis. — The prognosis depends upon the associated conditions. 
Sudden death may occur in kyphoscoliosis, and in bronchopneumonia 
in which change of posture, etc., does not lead to inflation of the collapsed 
areas. 

Treatment. — The treatment in general is that of the primary dis- 
order. In addition, measures that tend to prevent the development 
of the atelectasis should be employed. Thus, patients should be pre- 
vented from lying in the one position for a long time, and deep inspira- 
tions should be insisted upon from time to time. Cold affusions are 
of service in preventing the disorder, and of value when it has developed. 
Diffusible cardiac stimulants (camphor, ether, strychnine, ammonium 
preparations, etc.) are valuable, and so also sometimes are oxygen, 
compressed air, etc. In congenital atelectasis, forcible inflation has 
been productive of good results. 



BRONCHOPNEUMONIA 549 

BRONCHOPNEUMONIA. 

{Lobular Pneumonia; Capillary Bronchitis.) 

Bronchopneumon'a is a bacterial infection of the lungs characterized 
by inflammation of the terminal bronchioles and the related alveoli 
that collectively make up a lobule. It is not distinguishable from cap- 
illary bronchitis. 

Etiology. — Bronchopneumonia is most common in children under 
five years of age (75 per cent, of the cases) and in the aged; but adults 
are by no means exempt. It may occur at any season of the year, 
but it is especially prevalent during the winter and spring. Poor hygienic 
surroundings, malnutrition, etc., act as predisposing factors. The 
exciting causes comprise the pneumococcus, Friedlander's pneumo- 
bacillus, streptococci, staphylococci, the influenza bacillus, the typhoid 
bacillus, the tubercle bacillus, etc. The majority of cases are mixed 
infections. 

Primary and secondary cases may be distinguished. The primary 
cases are relatively uncommon; they occur particularly in previously 
healthy children under two years of age, and are usually due to the 
pneumococcus. The secondary cases are of several types: (1) Those 
complicating or following the infectious diseases, especially measles, 
pertussis, diphtheria, scarlatina, influenza, typhoid fever, etc., as well 
as other diseases attended by bronchitis. This group is especially 
common in children. In some cases of tuberculosis of the lungs of 
the ordinary chronic ulcerative type, bronchopneumonia (sometimes 
terminal) may develop, and is due frequently to the pneumococcus, 
although the lesions may be due to mixed infection. (2) Those com- 
plicating chronic debilitating disorders, such as nephritis, diabetes, 
chronic cardiac disease, prolonged confinement to bed (as in fracture 
of the femur), etc. This type is especially common in adults, partic- 
ularly the aged, and is often responsible for the final fatal issue, consti- 
tuting a so-called terminal infection. (3) Aspiration pneumonia, which 
occurs when the sensibility of the larynx has become benumbed, as in 
stuporous and comatose states, such as uremic or diabetic coma, apo- 
plexy, ether and chloroform anesthesia, or operations on the larynx or 
trachea, etc. — in which circumstances bacteria-laden particles of food, 
or saliva, etc., are drawn into the bronchi and ultimately set up inflam- 
mation. The pneumonia that may follow non-fatal drowning, the 
inhalation of irritating vapors, gases, etc., is perhaps of the same 
nature. (4) Perhaps in some cases the infection is carried to the lungs 
by the blood stream or the lymph stream. 

Pathology. — The lesions consist of scattered foci of solidification, 
varying in size from that of a pinhead to a cherry or larger; the foci 
are bilateral and usually most marked in the lower lobes. On section 
they consist of irregular, dark, reddish-brown (later, grayish or yel- 
lowish), firm, airless areas, in the centre of which a bronchiole can 



550 DISEASES OF THE LUNGS 

often be detected; it is usually filled with mucopus, and its epithelium 
is swollen and reddened. Surrounding vesicles are often atelectatic; 
perhaps in some cases the atelectasis precedes the inflammatory phe- 
nomena. Microscopically, the bronchioles show the ordinary vascular 
and exudative lesions of inflammation, especially cellular infiltration, 
and proliferation and desquamation of the epithelium, which, with 
the mucopus, obstructs the bronchioles; the related alveoli are more 
or less filled with leukocytes, some erythrocytic cellular exudation, pro- 
liferated and desquamated alveolar epithelium, and some fibrin forma- 
tion — which is most marked in the pneumococcic cases (although 
always less than in so-called lobar pneumonia), and less in pyococcic 
and influenzal cases, etc. ; the alveolar walls are swollen and infi - 
trated and show the ordinary lesions of inflammation. These dissemi- 
nated foci of peribronchial solidification and atelectasis, and embrac- 
ing areas of more or less well aerated lung, constitute the common 
type; in some cases bronchitis and bronchiolitis with comparatively 
little (although always some) alveolar involvement are the conspicuous 
lesions; whereas in other cases the lesions spread from the primary 
foci directly from one alveolus to adjacent alveoli or through the lym- 
phatics until more or less of the lobe is involved (pseudolobar form) ; but 
intervening areas of more or less congested pulmonary tissue separate 
the solidified lobules. The bronchopneumonic lesions may resolve 
(autolysis, fatty degeneration, etc.) and become absorbed, perhaps in 
part expectorated; or if death does not ensue from exhaustion and 
toxemia, pulmonary abscess, gangrene, or fibrosis may ensue. 

Symptoms. — In primary bronchopneumonia the onset may be sudden, 
following slight exposure (as in ordinary lobar pneumonia); there may 
be a chill (or chilliness, or perhaps a convulsion in young children), 
rapid rise of temperature, cough, and dyspnoea. In some cases the 
pulmonary symptoms are overshadowed by the general, or perhaps 
by unusual cerebral manifestations (stupor, coma, delirium, etc.). 
Secondary bronchopneumonia, following, for instance, one of the acute 
infections of children with bronchitis, is usually of insidious onset; 
it is characterized by exaggeration of the already existing fever, increased 
cough and dyspnoea, and cyanosis, any or all of which are indicative 
of bronchopneumonia in a susceptible bronchitic subject; rarely the 
onset is sudden. The fully developed disease is characterized by 
irregular fever (103° to 105°), rapid, feeble pulse (140 to 160 per minute 
in children), hard, ineffectual, and distressing cough, dyspnoea (60 
to 80 or more respirations per minute in children), activity of the acces- 
sory muscles of respiration, inspiratory retraction of the lower part of 
the chest, cyanosis, marked prostration, stupor (and other so-called 
meningitic manifestations), leukocytosis, etc. 

Physical Signs. — The physical signs in the early stages and in some 
cases throughout the course of the disease, consist of harsh broncho- 
vesicular (puerile) breath sounds and fine crackling and sibilant rales 
throughout both lungs; that is, signs of solidification are altogether 



BRONCHOPNEUMONIA 551 

wanting (the capillary bronchitis of some writers). In other cases 
there are in addition scattered foci of impaired resonance, sometimes 
of more or less well-marked dulness, and increased tactile and local 
fremitus, especially at the bases posteriorly; in the event of widespread 
involvement of a lobe more or less outspoken bronchial (tubular) 
breath sounds may be heard. 

Similar symptoms and physical signs develop in the event of aspiration 
or deglutition pneumonia. The bronchopneumonia that develops in 
adults in debilitated and cachectic states is often extremely insidious 
in onset; symptoms often are markedly in abeyance; there may be 
only a little dyspnoea, or perhaps cyanosis, and the disease may be 
overlooked unless the chest be examined. 

Diagnosis. — The diagnosis of the common secondary broncho- 
pneumonia of children should be based upon the primary disorder 
and the advent of increased fever, cough, dyspnoea, and cyanosis; the 
physical signs of solidification often may be entirely absent. Acute 
bronchitis may be differentiated by the low fever, less dyspnoea, and 
less cyanosis ; there is no clinical and little anatomical difference between 
capillary bronchitis and bronchopneumonia. Lobar pneumonia may 
be distinguished by its comparative rarity in infants, and its charac- 
teristic mode of onset, physical signs, and course. Efforts should 
always be made to determine the etiological factor in each case by 
examining the sputum. 

Prognosis. — The course of bronchopneumonia may rarely be acute, 
lasting about a week or ten days; usually it lasts from three to six or 
eight weeks or more. Death may ensue from divers complications, 
toxemia, or asthenia; recovery ensues by lysis. The prognosis should 
always be guarded, especially in the very young and the aged; it is 
especially bad in the cases following measles and pertussis in debilitated 
and rickety children, in aspiration pneumonias, and generally when 
there is marked cyanosis, dyspnoea, toxemia, and prostration. 

Treatment. — The treatment, in general, is that of the primary dis- 
order, or of acute bronchitis, or of croupous pneumonia. The most 
important measure, especially in young children, consists of an abundant 
supply of fresh, cool air, which, ordinarily, is best obtained by open win- 
dows or by roof gardens at hospitals, etc. Fresh, cool air stimulates the 
vasomotor system and the heart, relieves the cyanosis, and lessens the 
toxemia and its cerebral effects — and is much superior to canned oxygen 
in a warm, ill-ventilated room. The patient should be well protected by 
a sufficiency of, but not too many, bedclothes (remembering the fever) ; 
the feet should always be kept warm and the head cool. The patient 
should not be distressed by poultices, blisters, and other counter- 
irritants. If the physician must contend against local prejudices, 
let him apply a loose-fitting cotton jacket (which may take the place 
of other clothing). The diet should be fluid. An abundance of cold 
water should be given to drink. The bowels should be opened thor- 
oughly — castor oil or magnesia in children; calomel or blue mass and 



552 DISEASES OF THE LUNGS 

a saline cathartic in adults. The use of water externally and internally 
as recommended in croupous pneumonia, is serviceable; in children 
a warm bath is often better; in adults, as well as in children, the 
desired result of hydrotherapy is reaction and stimulation, and not 
reduction of temperature. Diffusible stimulants, such as whiskey and 
brandy, strychnine, ammonia, and camphor, comprise the really effica- 
cious remedies; coal-tar products and all depressing drugs should be 
absolutely avoided. Restlessness, pain, excessive cough, etc., suggest 
the use of bromides, Dover's powder, paregoric, etc., all of which should 
be used with caution in the young and the aged. The other therapeutic 
indications are similar to those mentioned under bronchitis and croupous 
pneumonia. 

CHRONIC INTERSTITIAL PNEUMONITIS. 

(Chronic Fibroid Pneumonia; Fibroid Induration of the Lung; Sclerosis of the Lung, 

Fibroid Phthisis.) 

Etiology. — Chronic interstitial pneumonitis may occur as a primary 
or a secondary process. The primary process is due to syphilis or to 
the inhalation of irritating dust (pneumokoniosis). The secondary 
process may follow croupous pneumonia, bronchopneumonia, tuber- 
culosis, collapse of the lung (due to an aneurysm, a tumor, etc.), chronic 
pleuritis, etc. A local fibrosis is common in association with healed 
foci of tuberculosis, especially at the apex, gummas, pleural thickenings, 
gangrene, tumors, hydatid cysts, etc. 

Pathology. — The lesion may be localized or diffuse, unilateral or 
bilateral. They consist of proliferation of the fibrous connective tissue, 
which begins in the interlobar or interlobular septa or about the bron- 
chioles, depending upon the variety of the disease. In the form that 
follows croupous pneumonia the exudation, instead of undergoing 
autolysis, becomes organized; fibroblasts invade it and ultimately lead ■ 
to a fibrillar thickening of the alveolar walls and obliteration of many 
of the alveoli. The affected portion of the lung is contracted, smooth, 
firm, dense, homogeneous, semitranslucent, grayish white in color, 
and almost if not quite airless. Often an entire lobe is involved, in which 
event it may be much reduced in size and lie against the spine as an 
irregular, dense mass. In the form that follows bronchopneumonia, 
the fibrosis begins about the bronchi; the alveolar walls become much 
thickened, and small foci, lobular masses, smooth, firm, grayish in color, 
are found scattered throughout a lobe or an entire lung. On section 
these areas usually reveal a central bronchiole. From contraction of 
the newly formed fibrous tissue bronchiectasis not infrequently results. 
The pleurogenous form may follow prolonged compression of a lung 
by a pleural exudate; in other cases bands of fibrous connective tissue 
extend from the pleura (sometimes only the interlobar pleura) a variable 
distance into the lung, and by cicatrization lead to compression and 
atrophy of the lung tissue, and to bronchiectasis. At times the lung 



CHRONIC INTERSTITIAL PNEUMONITIS 553 

consists virtually of a series of bronchiectatic cavities, in the walls of 
which aneurysmal dilatations of the pulmonary artery are not uncommon. 
Bronchitis (fibrous peribronchitis) is a part of the general process of 
indurative pneumonitis. Tuberculosis may ensue. The uninvolved 
portion of the lung, or the opposite lung, is commonly the seat of com- 
pensatory inflation. The heart is often displaced, retracted toward the 
diseased side; the right ventricle is usually hypertrophied. 

Symptoms.- — The symptoms are often merged with those of the primary 
disorder — croupous pneumonia, bronchopneumonia, pleuritis, etc. The 
patient does not fully recover — slight cough, mucopurulent expectoration, 
dyspnoea, and perhaps a little fever persist for some time. Gradually 
the symptoms become only those of chronic bronchitis; later, usually 
those of bronchiectasis, which with the physical signs of retraction of 
the chest are quite characteristic of the disease. 

Physical Signs. — The chest is depressed over the affected lung or part 
of the lung; the interspaces are obliterated; the ribs may overlap; the 
shoulder is depressed; the nipple and the scapula are nearer the median 
line; scoliosis even may develop. The inspiratory expansion of the chest 
is restricted; that of the unaffected lung may be increased. The tactile 
and the vocal fremitus are increased. On percussion there is dulness 
or a vesiculotympanitic sound (bronchiectatic cavity). On auscultation 
there is harsh bronchovesicular breathing, or the breath sounds are 
feeble (thickened pleura, etc.); and crackling, sibilant, sonorous, and 
bubbling rales and sometimes pleural frictions may be heard. Retrac- 
tion of the left lung by uncovering the heart causes an increase in the 
area of cardiac dulness (some of the increase is due to hypertrophy and 
dilatation of the right ventricle), increased visible and palpable pulsa- 
tion of the heart and adjacent vessels (pulmonary artery and the 
aorta), palpable closure of the pulmonary valve, increase of the 
tympany of Traube's semilunar space; etc. Retraction of the right 
lung causes displacement of the heart to the right, elevation of the 
liver, etc. 

Diagnosis. — Usually for some time the diagnosis is that of the primary 
disorder, or of bronchitis. With the development of retraction of the 
chest the diagnosis becomes quite obvious. Tuberculosis should be 
excluded. 

Prognosis. — Although the disease is incurable, the patient may live 
many years and enjoy tolerably good health. Exacerbations of the 
bronchitis are not uncommon. Death usually results from progressive 
toxemia (bronchiectasis), failure of the right heart, or some intercurrent 
infection (bronchopneumonia, etc.). 

Treatment. — The treatment is that of chronic bronchitis and bronchi- 
ectasis. A nutritious diet and the best hygienic and climatic conditions 
are of prime importance. 



554 DISEASES OF THE LUNGS 

PNEUMOKONIOSIS. 

(Anthracosis; Chalicosis; Siderosis.) 

Etiology. — Pneumokoniosis is a term applied to the fibroid and other 
changes in the lungs that result from the inhalation of various kinds of 
dust. The condition is essentially an occupation disease, and is seen 
especially in those constantly exposed to dust-laden atmosphere. Dif- 
ferent varieties of the disease are distinguished, depending upon the 
nature of the dust inhaled: (1) Anthracosis, that due to the inhalation 
of carbonaceous pigment, coal dust, soot, charcoal, etc. (coal-miner's 
disease, or phthisis) ; (2) chalicosis, that due to the inhalation of silicious 
dust, such as sandstone, quartz, etc. (stone-cutter's phthisis, millstone 
maker's phthisis, grinder's and potter's rot or asthma); (3) siderosis, 
that due to the inhalation of mineral dust, especially iron oxide, brass, 
bronze, etc.; (4) that due to the inhalation of particles of wool, flax, 
cotton, etc.; and (5) that due to the inhalation of grain dust, cereals, etc. 
(miller's phthisis). Associated bacterial infection is doubtless of some 
significance. 

Pathology. — Small amounts of dust being inhaled are absorbed by 
phagocytes (leukocytes and other cells), which then are carried upward 
by the ciliated epithelium and expectorated. When larger amounts are 
inhaled, some penetrates to the mucosa of the small bronchi, where it is 
attacked (engulfed) by the normal scavengers of the respiratory tract, 
the mucous, and the alveolar cells. When the amount of the dust is 
excessive some of it reaches the alveoli, and some of it penetrates the 
mucosa and reaches the lymph stream. In this event it may be carried 
to the lymph nodes surrounding the bronchi and bloodvessels, to the 
interlobular septa beneath the pleura, and to the substernal, bronchial, 
and tracheal lymph nodes. Rarely the dust particles gain the general 
circulation, and may be found in the liver, spleen, kidney, mesenteric 
and retroperitoneal lymph nodes, etc. — cases in which the pigmented 
bronchial nodes have formed an intimate connection with the pulmonary 
veins and permit the passage of dust-laden cells into the veins. In the 
large majority of cases there is no reaction to the deposit of these foreign 
bodies in the lung, and the lungs show no noteworthy deviation from the 
normal, aside from variations in color depending upon the special pig- 
ment deposited (black, coal dust; whitish or grayish, stone dust; yellowish, 
reddish, or black, iron dust). In some cases, however, reaction does 
take place: this consists of the proliferation of fibrous connective tissue 
beginning in the peribronchial lymph nodes, to which it may remain 
localized — in which event the fibroid nodules appear as firm, hard, 
circumscribed masses, varying in size from a millet seed to a cherry, 
scattered throughout both lungs, and on section revealing in the centre a 
bronchiole. In other cases the process is more diffuse, and involves 
almost, if not quite, an entire lobe. In these cases there is also thick- 
ening of the alveolar walls and of the interlobular and perivascular 



EMPHYSEMA 555 

tissue, so that the affected portion of the lung is contracted, dense, firm, 
and almost airless; in some areas the bronchi and alveoli may be com- 
pletely obliterated. An important element in the process is the asso- 
ciated bronchitis (which causes most of the symptoms) and emphysema; 
bronchiectatic cavities are common; in other cases necrosis of affected 
areas takes place and leads to the formation of cavities with irregular 
and roughened walls, traversed by fibrous bands, communicating or 
not with a bronchus, and containing thick, dark, sometimes blood- 
stained fluid. Tuberculosis is a common sequel. 

Symptoms. — The symptoms are those of chronic bronchitis and 
emphysema — cough, dyspnoea (especially on exertion), and expectora- 
tion, which, however, do not come on until the subject has worked in 
the dust for a number of years. The expectoration is usually profuse, 
mucopurulent, and blackish in anthracosis; in chalicosis one may detect 
microscopically angular crystalloid particles of silica; and in siderosis, 
yellowish or reddish particles of iron oxide. In the course of time the 
general health begins to fail, and the patient may become much emaciated. 

Physical Signs. — The physical signs are those of chronic bronchitis 
and emphysema; later, those of chronic induration of the lung, and cavity 
formation. 

Diagnosis. — The diagnosis is usually easy, if the patient's occupation 
is taken into account. Cavities should not be misinterpreted as tubercu- 
lous necessarily; tubercle bacilli may be absent throughout the entire 
course of the disease. 

Prognosis. — The prognosis as regards life expectancy is rather good. 
The patient may survive many years. Death often results from secondary 
tuberculous or other infection (bronchopneumonia, etc.). The develop- 
ment of bronchiectasis and excavation renders the prognosis unfavorable. 

Treatment. — The treatment is that of chronic bronchitis and emphy- 
sema. The patient should give up his occupation if possible; if this be 
impossible, he should spend considerable time in the open air. 



EMPHYSEMA. 

Emphysema is a chronic disease of the lungs characterized by perma- 
nent overdistention of the air vesicles and atrophy of the vesicular 
walls. 

Etiology. — True (large-lunged, pseudohypertrophic) emphysema is 
peculiarly a disease of adult life, although well-marked examples are 
occasionally seen in children. It is most common in the male sex. In 
some cases it seems to be predisposed to by heredity (hereditary weak- 
ness of the pulmonary elastica and consequent deficiency of contractile 
power). It is especially common in those whose occupation requires 
prolonged increase of intrapulmonary pressure with a closed glottis 
and muscular effort, such as players on cornets and other wind instru- 
ments, glassblowers, and those that lift or move heavy bodies (pianos, 



556 DISEASES OF THE LUNGS 

etc.). Advancing age is a predisposing factor, but this usually results 
in so-called senile (small lunged) emphysema. The disease is especially 
common as a secondary process in diseases attended with violent cough- 
ing spells and difficulty in expiration, such as pertussis, chronic bronchitis, 
asthma, etc. In these there is always obstruction to the exit of air 
through the bronchioles and consequent increased intra-alveolar pres- 
sure, which becomes markedly augmented during the violent expirating 
efforts of coughing. 

Pathology. — Both lungs are obviously enlarged, filling an enlarged 
thorax, depressing the diaphragm, and overlapping the heart; they are 
pale and anemic (aside from the common anthracosis), and characteris- 
tically light and downy to the touch; that is, despite the obvious increase 
in size, there is a lack of pulmonary tissue. Larger or smaller bullae 
(coalescence of several alveoli) may be seen at different parts of the 
lungs, but especially at the free margins, anteriorly and basally (which 
become rounded), and the apices (less well supported than elsewhere), 
and that portion in the vertebral fossae. The conspicuous lesions con- 
sist of dilatation of the alveoli and infundibula; atrophy of the inter- 
alveolar walls, including the elastica; consecutive thrombosis and oblit- 
eration of the interalveolar capillaries and also the lymphatics; fatty 
and other degenerative processes of the epithelial lining of the alveoli; 
and the eventual establishment of abnormal communications between 
adjacent dilated alveoli. The bronchi and bronchioles show the common 
lesions of chronic inflammation — being thickened, indurated, dilated, 
and distorted. There is more or less thickening and sclerosis of the 
pulmonary artery, which together with restriction of the arterial tree 
from capillary thrombosis, leads to hypertrophy of the right ventricle; 
the increased tension in the pulmonary artery is somewhat relieved 
by normal communications between the pulmonary artery and the 
pulmonary and bronchial veins — but this leads to increased cyanosis, 
since the blood thus diverted does not become well aerated. 

There is still doubt regarding the real nature of the process. Although 
some observers still hold that it results from inspiratory distention or from 
primary degenerative changes of the alveolar walls, the prevailing view is 
that it is due to expiratory difficulties and consequent increase in intra- 
alveolar pressure — which becomes especially significant etiologically when 
acting upon lungs reduced in resisting power by hereditary influences, 
chronic inflammation (bronchitis), senility, etc. At the time of greatest 
intra-alveolar pressure (at the acme of coughing, straining, etc.) the 
lungs are inflated to the maximum, the glottis is closed, and the thorax 
fixed, so that air is forced into parts of the lungs normally slightly 
expanded, that is, the apices and the anterior margins, which being also 
ill supported, feel the strain most and reveal the most marked lesions. 
In consequence of repeated insults, the pulmonary tissue gradually loses 
its elasticity, and the lungs gradually become permanently almost, if not 
quite, maximally distended ; and the chest, permanently in the condition 
of inspiratory expansion, assumes the characteristic barrel-shape. Some 



EMPHYSEMA 557 

observers have postulated primary ossifying changes in the costal car- 
tilages. 

Symptoms. — The significant symptoms of emphysema are progres- 
sive dyspnoea and cyanosis. At first these are noticeable only on severe 
exertion, but as the disease advances they develop on the slightest exer- 
tion and then become permanent. The dyspnoea is chiefly expiratory, 
and is increased by mental excitement and bodily exertion. The respi- 
rations are increased in frequency (20 to 30), and ultimately orthopncea 
supervenes. Cyanosis is an early and prominent symptom, apparent 
first in the lips, nose, ears, and extremities, but becoming more marked 
as the disease advances; it is often of a strikingly high grade, without 
notable discomfort to the patient. It is due in part to the disease of the 
lungs, in part also to failing cardiac compensation (dilatation ensuing 
upon the hypertrophy due to the pulmonary disease). Usually there 
is a co-existing bronchitis, which becomes aggravated in the winter, 
and occasions cough and mucopurulent expectoration; asthmatic 
attacks are common. So long as the hypertrophy of the right ventricle 
continues efficient the patient is tolerably comfortable; but eventually 
dilatation and failure of compensation ensue, whereupon increased 
dyspnoea and cyanosis, pulmonary oedema, and signs of general venous 
engorgement are likely to supervene. 

Physical Signs. — The aspect of the patient is often quite character- 
istic: if the disease is at all advanced he is markedly cyanotic and more 
or less dyspnceic, his eyeballs bulge, his head is thrown back and the 
chest forward, and the accessory muscles of respiration are active. 
The chest is characteristically barrel-shaped — shortened and increased 
anteroposteriorly; the neck is short and thick; the supraclavicular fossae 
may bulge; the sternum is prominent, the costal angle increased; the 
shoulders are raised and rounded, the ribs almost horizontal, and the 
intercostal spaces widened and depressed. The movements of the 
chest are vertical rather than expansile; the inspiratory movements 
are shortened, the expiratory prolonged; respiration is carried on largely 
by the diaphragm and the abdominal muscles, although the excursions 
of the diaphragm are restricted (obvious by the use of the cc-rays and 
in the limitation or absence of Litten's diaphragm sign). A line of 
distended capillaries and venules around the chest often marks the 
attachment of the diaphragm. The percussion note is hyperresonant 
or vesiculotympanitic; in some places dull (imperfect resonance of the 
thorax due to tension or ossifying costal cartilages). The increased 
volume of the lungs is revealed in percussion resonance to the seventh 
rib or below in the mamillary line and to the first or second lumbar 
spine posteriorly, by reduction in size and eventual obliteration of the 
superficial cardiac dulness, encroachment of resonance on the hepatic 
and splenic dulness, pulmonary resonance in Traube's semilunar space, 
and little or no respiratory movement of the lower limits of pulmonary 
resonance (in Gerhardt's space and at the cardiopulmonary borders). 
The breath sounds are weakened, sometimes almost inaudible, and 



558 DISEASES OF THE LUNGS 

the expiration is much prolonged in uncomplicated emphysema; with 
complicating bronchitis, the breath sounds are usually harsh and broncho- 
vesicular in character, and rales may be heard. Adventitious sounds 
may also be due to shifting of air in emphysematous bullae, pulmonary 
oedema, muscular contractions, etc. The cardiac apex is usually not 
to be seen or felt; a common palpable pulsation in the epigastrium 
results from downward displacement of the heart and hypertrophy 
of the right ventricle. The heart sounds are weak and indistinct, and 
there may be a systolic murmur (cardiopulmonary; relative tricuspid 
or mitral insufficiency). 

Diagnosis. — The disease is readily recognized from the history and 
the physical signs, although minor grades are often overlooked or mis- 
interpreted. The cyanosis, dyspnoea, and a possible systolic murmur 
should not be mistaken for primary cardiac disease; the other physical 
signs are unequivocal. Pneumothorax is sometimes confused, on 
account of the clear vesiculotympanitic percussion rate. 

Senile Emphysema — In contradistinction to the so-called large 
lunged emphysema, a small lunged (atrophic or senile) emphysema 
is often encountered in elderly people. This is a primary atrophy of 
the pulmonary tissues, part of the general atrophy of senility. It is 
attended by some dyspnoea, but not much cyanosis ; there may or may not 
be cough, but if present it is not marked. The chest is small and flat; 
the normal obliquity of the ribs is perhaps accentuated; the muscula- 
ture is atrophic; the normal type of breathing is maintained; the percus- 
sion note is hyperresonant, and the breath sounds are weak, unless 
there be associated bronchitis. 

Compensatory Inflation (Vicarious Emphysema). — In local 
disease of the lungs, such as pneumonia, bronchopneumonia, more or 
less quiescent tuberculosis, chronic fibrosis, pleural adhesions, pleural 
effusion, parts of the lung adjacent to the diseased foci, or a lobe, or 
the opposite lung, takes on a compensatory process, becomes distended — 
so-called compensatory emphysema (preferably inflation or distention). 
This is at first a purely physiological process — enlargement of the 
alveoli, but no atrophy of the walls ; it is believed to be inspiratory rather 
than expiratory in development; it may be temporary, and, as in pneu- 
monia or pleural effusion, subside with the subsidence of the primary 
disorder, but if long continued, true emphysema may ensue. 

Acute Vesicular Emphysema. — Acute vesicular emphysema (or dis- 
tention) sometimes ensues when violent inspiratory efforts have been 
made in conditions of bronchial obstruction, especially in bronchitis of 
the fine tubes, asthma, pertussis, aortic aneurysm, etc. The percussion 
note is hyperresonant and more widely distributed than normally, the 
expiration is prolonged, and there are many sonorous and sibilant 
rales. It is readily distinguished by its usually acute onset, associated 
phenomena, and common subsidence. 

Interstitial Emphysema. — Interstitial (interalveolar, interlobular, 
or subpleural) emphysema is a condition characterized by the presence 



ABSCESS OF THE LUNG 559 

of air in the interstices of the lung, where it forms larger or smaller 
bullae. It may be due to trauma (fracture of the ribs, punctured 
wounds of the chest, tracheotomy, etc.); rupture of the air vesicles 
from overdistention (severe paroxysmal coughing, straining of parturi- 
tion or defecation, etc.); it may follow pneumothorax, subcutaneous 
emphysema of the neck, ulceration of the air passages and pulmonary 
tissue, etc. The air enters the pulmonary tissue by means of a tear in 
the alveoli or bronchi. In mild cases symptoms may be in abeyance; 
in severe cases there may be very urgent dyspnoea and cyanosis, usually 
of sudden onset (diagnostic importance of the etiological factors). Ex- 
amination may reveal intrathoracic creaking and crepitation (perhaps 
synchronous with the action of the heart), obscuration of the heart 
dulness and sounds and of the breath sounds, and sometimes large 
areas of tympany, etc. 

Prognosis. — True emphysema is a disease of long duration, upward 
of twenty years in many cases. Complete recovery is scarcely to be hoped 
for, but the patient may be much benefited, his condition made bearable, 
and his life prolonged. Death usually results from cardiac failure or 
secondary infections, such as pneumonia, bronchopneumonia, tuber- 
culosis, hemoptysis, etc. 

Treatment. — The treatment virtually is that of chronic bronchitis. 
Efforts should be made to improve the patient's general health; he 
should lead a hygienic life, avoid the causative factors (blowing wind 
instruments, etc.) if these be detectable, and avoid also lifting heavy 
weights and other severe exertion, as well as cold and the taking of cold. 
Life in a warm, equable climate is of the greatest service. In the absence 
of this, respiratory exercises, which increase the force of expiration, 
systematic rhythmic compression of the thorax, compressed air baths, 
and the breathing of rarefied air are valuable. Many patients are 
remarkably improved by the iodides, in addition to the remedies men- 
tioned for chronic bronchitis. In other cases alleviation of the cardiac 
inadequacy is followed by much benefit; as a matter of fact in moderately 
or well-advanced cases the cardiac factor in the symptomatology is 
often overlooked; small doses of strophanthus or digitalis, and other 
measures recommended in failing cardiac compensation, often lead to 
material relief. In the event of unusual cyanosis and dyspnoea vene- 
section is called for. Attention should be paid to the diet to obviate 
gastro-intestinal derangements and to correct them if they develop. 
General tonics, such as iron, strychnine, etc., are useful from time to 
time. 



ABSCESS OF THE LUNG. 

Etiology. — Abscess of the lung most frequently follows croupous 
pneumonia, aspiration pneumonia, and infectious embolism. Less com- 
monly it follows ordinary bronchopneumonia, and other diseases of the 



560 DISEASES OF THE LUNGS 

lung, such as tuberculosis, fetid bronchitis, bronchiectasis, glanders, 
actinomycosis, etc. Occasionally it results from extension of suppura- 
tion from adjacent tissues and organs, such as empyema, mediastinal 
abscess, suppurating bronchial lymph nodes, vertebral abscess, sub- 
diaphragmatic abscess, hepatic abscess, etc. Traumas, perforating 
wounds of the lung, etc., also are likely to lead to abscess. The dis- 
ease is much more common in debilitated than in healthy subjects; 
diminution of general bodily resistance seems to be of considerable 
etiological importance. Staphylococci, streptococci, pneumococci, pneu- 
mobacilli, influenza bacilli, typhoid bacilli, colon bacilli, leptothrix, etc., 
are the bacteria commonly encountered in the abscess. 

Pathology. — There may be a single abscess (following croupous 
pneumonia), or there may be many abscesses (following infectious 
embolism). The single large abscess may involve an entire lobe, or 
an entire lung. When multiple, the abscesses are usually small, varying 
in size from that of a pea to that of a walnut, wedge-shaped, and super- 
ficial; the cavity is irregular, its walls ragged, its contents purulent, and it 
may contain considerable necrotic lung tissue. The large single abscesses 
present similar appearances on a more extensive scale. When the abscess 
reaches to the periphery the superjacent pleura is commonly covered 
with a fibrinous exudation. Perforation of the abscess into a bronchus 
and the discharge of its contents externally is not uncommon. Per- 
foration may also occur into the pleura (causing empyema or pyopneu- 
mothorax), or into the pericardium, etc. When old, the walls of the 
abscess cavity may be very thick, and bands of cicatrizing connective 
tissue may extend varying distances into the lung. 

Symptoms. — The symptoms are often for some time obscured by those 
of the primary disorder — pneumonia, sepsis, etc. The small multiple 
abscess may remain altogether undetected. The larger abscesses, 
those following pneumonia, for instance, are often suggested by the non- 
occurrence of the crisis and an aggravation of the general symptoms, 
septic temperature, chills, sweats, leukocytosis, etc. But the diagnosis 
may not be certain until the appearance of the characteristic sputum — 
purulent, yellowish, greenish, or brownish (from admixture of blood), 
malodorous (though never as fetid as in gangrene or fetid bronchitis, 
and occasionally having little or no odor), and containing fragments of 
necrotic lung tissue, elastic fibers, fatty acids, hematoidin crystals, bac- 
teria, etc. Sometimes a large amount of purulent sputum is expectorated 
at one time, whereupon the physical signs of cavity formation may 
become apparent — in which event the diagnosis is no longer in doubt. 
Often large amounts of sputum are raised early in the morning, or at 
other times upon the assumption of some particular posture (which 
favors drainage). 

Diagnosis. — The diagnosis, as a rule, is easy when the symptoms and 
signs are fully developed — the history, the fever and other signs of sepsis, 
the leukocytosis, the characteristic sputum, and the physical signs of 
cavity formation,. 



GANGRENE OF THE LUNG 561 

Prognosis.— The prognosis is always grave. Recovery sometimes 
takes place when the abscess has followed pneumonia or empyema. 
Multiple abscesses are generally part of a pyemic process that leads 
to death. 

Treatment. — As a rule, medicinal treatment is of minor importance, 
and consists of attention to the general health of the patient, the ad- 
ministration of stimulants, such as iron, quinine, strychnine, whiskey, 
etc., and the use of nutritious food. Hope of success lies in surgical 
measures which should be undertaken as soon as the abscess can be 
definitely localized. 



GANGRENE OF THE LUNG. 

Etiology. — Gangrene, the putrefaction of necrotic lung tissue, occurs 
under a variety of circumstances. An essential factor appears to be 
reduction in the general bodily resistance, whence it is found especially 
in debilitated subjects, alcoholics, diabetics, syphilitics, after severe infec- 
tious diseases (typhoid and typhus fevers, smallpox, scarlatina, etc.), in 
the subjects of severe mercurial and lead poisoning, etc. It follows a 
variety of local disorders in the lung, of which the most important are 
the different forms of pneumonia, especially, however, aspiration pneu- 
monia following the entrance of foreign bodies in a bronchus. The 
secretion in putrid bronchitis, the contents of a tuberculous or bron- 
chiectatic cavity, or of a lung abscess or a necrotic echinococcus cyst, 
etc., may induce gangrene in adjacent parts of the lung. A similar 
result may follow rupture into a bronchus or the lung of an empyema, 
a carcinoma of the oesophagus or the stomach, a gastric ulcer and 
subdiaphragmatic abscess, or a vertebral abscess. Infectious embolism 
or infection of a benign embolus, pressure of an aneurysm of the aorta, 
perforating wounds of the lungs and other traumas, etc., also may lead 
to gangrene of the lung. Staphylococci, streptococci, colon bacilli, 
Bacillus pyocyaneus, Micrococcus tetragenus, and the leptothrix are the 
organisms most commonly found in lung gangrene. 

Pathology. — Two forms of gangrene may be distinguished: (1) The 
circumscribed, and (2) the diffuse. The circumscribed form is more 
common in the lower lobes, and in the right lung; but it may be bilateral; 
the diffuse form is most common in the right upper lobe. The diffuse 
form is very rare, and occurs usually after lobar pneumonia, bronchitis, 
or embolic obstruction of a large branch of the pulmonary artery. The 
gangrenous area, which may involve an entire lobe, may be indistinctly 
outlined, firm, and greenish black in color; more commonly it is soft, 
pulpy, and extremely fetid; with the progress of the process large cavities 
are formed, traversing which the remains of bronchi and bloodvessels 
may be seen. The surrounding lung tissue exhibits the changes of well- 
marked inflammation. The circumscribed form occurs most commonly 
after multiple infarction or aspiration pneumonia. The foci of gangrene 
36 



562 DISEASES OF THE LUNGS 

are multiple and reach often to the pleural surface of the lung; they 
are usually rather sharply circumscribed, irregular in shape, greenish 
black in color, and extremely malodorous; as the process advances, 
irregularly shaped cavities with shreddy walls are formed. Should 
these cavities communicate with a bronchus, as occasionally happens, 
their contents may be expectorated. The foci of gangrene are surrounded 
by areas of inflammation; later they may become sequestrated and 
encapsulated, and healing may ensue. Occasionally, rupture into the 
pleura occurs, with the development of pyopneumothorax. Metastatic 
emboli, especially to the brain, are not uncommon. 

Symptoms. — The characteristic symptoms consist of fetid expectora- 
tion and fetor of the breath; but these do not develop until the putrefying 
lung tissue communicates with a bronchus. The symptoms, therefore, 
for some time are those of the primary disease. The gangrene may be 
inaugurated by chills, high fever, and marked prostration. Soon, how- 
ever, fetor of the breath is observed, especially after coughing, and the 
sputum becomes characteristically fetid, and abundant, and when 
allowed to stand separates into three layers — an uppermost discolored, 
frothy layer; a middle clear, greenish or brownish, serous or mucous 
layer; and a lowermost layer (sediment), consisting of necrotic lung 
tissue, pus, fibrin, elastic tissue, fatty acids, tyrosin, bacteria, etc. Occa- 
sionally there is also blood. As a rule, the patient becomes markedly 
prostrated, emaciated, and septic, and soon dies of exhaustion or a severe 
hemorrhage. 

Physical Signs. — The physical signs are often obscured by those of the 
primary disease. Distinctive signs consist of evidences of solidification 
(circumscribed foci or a large area) followed by those of excavation. 

Diagnosis. — The diagnosis virtually rests upon the fetor of the breath 
and of the expectoration — which can scarcely be mistaken. Abscess 
of the lung may be excluded by an examination of the sputum. Fetid 
bronchitis may be distinguished by its slower course, less fetor, and 
absence of lung tissue in the sputum. 

Prognosis. — The prognosis is grave. Death usually ensues, but re- 
covery may take place — less likely in the diffuse than in the circum- 
scribed form. 

Treatment. — Treatment is usually limited to supporting the patient by 
good nutritious food and the use of stimulants — iron, quinine, whiskey, 
strychnine, etc. Efforts should be made to lessen the fetor by sprays 
of carbolic acid, or by inhalation, of creosote, carbolic acid, guaiacol, etc. 
If the gangrenous area can be accurately localized, recourse may be 
had to surgical intervention with a view to drainage, and with hope of 
good result. 

TUMORS OF THE LUNG. 

Etiology. — Tumors of the lung may be primary (rare) or secondary 
(more common). Their etiology is that of tumors in general. Of the 



TUMORS OF THE LUNG 563 

primary tumors, carcinomas developing from the bronchial mucosa 
(cylindrical epithelioma) or from the alveolar epithelium (squamous, 
medullary, or scirrhus carcinoma) are the most common; sarcoma 
(lymphosarcoma, round-cell, spindle-cell) and endothelioma, develop- 
ing from the bronchial lymph nodes or the interstitial tissue of the 
lung, are less common; still rarer are fibromas, chondromas, osteomas, 
lipomas, lymphomas (of Hodgkin's disease), etc. Secondary tumors 
comprise carcinoma, sarcoma, endothelioma, and hypernephroma. The 
primary growths occur with greatest frequency in the breast, the diges- 
tive tract, the genito-urinary tract, and the bones. Metastasis to the 
lungs occurs usually by way of the bloodvessels, unless the primary 
growth is situated near the root of the lung, in the oesophagus, for 
instance, when metastasis may occur by way of the lymphatics. 

Pathology. — Primary tumors generally involve one lung (the right), 
and the upper lobe more frequently than the lower; but they may involve 
both lungs. They may occur as small, firm, sharply circumscribed 
masses, or as large infiltrating masses. Primary carcinoma is usually 
a large, firm, whitish or grayish mass, often sharply circumscribed; 
sometimes a diffuse infiltrating mass; sometimes a series of small nodules, 
distributed from the hilum along the bronchi and the vessels by way 
of the lymphatics. Often these nodules reach the pleura, where they 
form flat irregular masses; marked thickening of the pleura may occur. 
Carcinoma shows a tendency to soften and to give metastasis (80 to 90 
per cent, of the cases) to the adjacent lymph nodes, mediastinum, liver, 
brain, bones, etc. Secondary carcinoma occurs as small miliary or 
larger whitish or grayish nodules (resembling tubercles) scattered 
throughout both lungs. Rarely they involve only the pleura. Sarcoma 
presents much similar appearances. With the tumor of the lung there is 
often associated bronchitis, bronchiectasis (with hemorrhagic transudate), 
etc. 

Symptoms. — The primary growth may cause no distinctive symptoms 
until it is far advanced. When there is extensive involvement of the 
lung there is usually substernal oppression, cough, dyspnoea, some- 
times fever and sweats, and later emaciation. In addition there are 
many symptoms referable to irritation and pressure by the growth — 
cough (bronchitis or pressure on the bronchus); pain (involvement of 
the pleura); dyspnoea (pressure on the trachea); changes in the voice 
(pressure on the recurrent laryngeal nerve); slow pulse or rapid pulse 
(pressure on the pneumogastric nerve) ; cyanosis and oedema of the face 
or an arm (pressure on the veins); etc. The sputum is often quite char- 
acteristic, resembling red-currant jelly or prune juice; it may contain 
shreds of the pulmonary growth. Ultimately the patient becomes 
anemic and cachectic and dies of exhaustion. Secondary growths in 
the lungs are suggested by the development, in one who has or has had 
a primary tumor, of cough, dyspnoea, cyanosis, and blood-stained 
sputum; but since the primary growth is not always apparent, the diag- 
nosis may be for a long time in abeyance, 



564 DISEASES OF THE PLEURA 

Physical Signs. — The physical signs depend upon the size and seat 
of the tumor. At times there are only the signs of bronchitis; again, 
only moderate impairment of the percussion resonance. When the 
growth is extensive there may be fixation of the affected side (with 
compensatory activity of the other side), prominence of the affected 
side or distinct bulging, and widening of the interspaces. The percussion 
note may be normal when the foci are small and scattered; when there 
is a large localized mass there is dulness, which usually is very irregular 
in outline. Fremitus and the breath sounds may be diminished (blockage 
of the bronchi), or increased, that is bronchial breathing (unobstructed 
bronchi). The adjacent viscera (heart, liver, spleen, etc) may be dis- 
placed. The signs of pleural effusion may develop. The supraclavicular 
or the axillary lymph nodes may become enlarged (sometimes the first 
trustworthy clue to the correct diagnosis). 

Diagnosis. — The diagnosis is often difficult, especially in the primary 
cases. In the secondary cases, attention to the history of the patient and 
a study of the symptomatology and physical signs often suffice for a 
correct diagnosis. Care should be taken to exclude bronchitis, chronic 
interstitial pneumonia, tuberculosis, pleurisy with effusion, etc. 

Prognosis. — The prognosis is hopeless. Death usually ensues within 
a year or eighteen months. 

Treatment. — The treatment consists in humanitarian efforts to pro- 
mote the comfort of the patient and relieve his distressing symptoms. 



DISEASES OF THE PLEURA. 

PLEURITIS. 

(Pleurisy.) 

Pleuritis may be variously classified; it may be primary (rarely) 
or secondary (usually); acute or chronic in onset and course; circum- 
scribed or diffuse; fibrinous, serofibrinous, purulent, or hemorrhagic as 
regards the character of the exudate; and tuberculous, streptococcic, 
staphylococcic, pneumococcic, etc., as regards the specific etiological 
factor. Inasmuch as an etiological classification is scarcely feasible at 
the bedside, the following clinical classification will be found serviceable : 
acute and chronic pleuritis; of the acute, the following forms: fibrinous, 
serofibrinous, purulent, and hemorrhagic; and of the chronic forms : serous 
and adhesive. 



FIBRINOUS PLEURITIS. 

(Dry, Plastic, or Acute Adhesive Pleurisy.) 

Etiology. — Dry or fibrinous pleuritis seems to occur sometimes as an 
independent, or primary, disorder following exposure to cold and damp, 



FIBRINOUS PLEURITIS 565 

especially in alcoholic subjects; in most cases, however, it is a secondary 
process. It is most common in frank or latent pulmonary tuberculosis, 
but occurs also in other diseases of the lungs, such as bronchitis, pneu- 
monia, bronchopneumonia, pulmonary abscess and gangrene, etc.; 
in infections of adjacent organs, such as pericarditis, endocarditis, 
mediastinitis, disease, including traumatism, of the bony framework 
of the chest, etc.; in distant infections (hemogenic infections), such as 
of the abdominal and pelvic organs, tonsillitis, etc.; in general infec- 
tions, such as septicopyemia, rheumatism, typhoid fever, influenza, etc. ; 
and it is a common occurrence in debilitated and asthenic states generally, 
such as advanced cardiac and renal disease, etc. The specific etiological 
factor is usually the tubercle bacillus, less commonly staphylococci, 
streptococci, pneumococci, etc. 

Pathology. — The lesions may be more or less diffuse, but they are 
usually circumscribed, especially to the base of the lungs anteriorly and 
laterally, but often also at the apex (frequently overlooked). The 
inflamed area becomes hyperemic, swollen, lustreless, and finally 
granular in appearance; and the seat of a more or less abundant, thick 
or thin, usually slightly adherent fibrinous exudation. In reality the 
exudation is serofibrinous, that is, there is always some fluid exudation, 
but this is often minimal (dry pleurisy), and the excess of fibrin causes 
agglutination of the opposed pleural surfaces. Ultimately the exudation 
undergoes organization with the formation of permanent adhesions and 
pleural thickening. 

Symptoms. — Symptoms may be almost if not entirely in abeyance, 
since pleural adhesions constitute a very common necropsy finding 
apparently unassociated with notable symptoms during life. In some 
cases, however, especially following exposure, or traumatism of the 
chest, or in the course of tuberculosis, etc., there is a sudden pain in the 
side (pleural stitch), perhaps slight cough (which, as well as deep inspi- 
ration, increases the pain), and slight fever. The pain may occur at the 
site of inflammation, or laterally or anteriorly where the movement of 
the lung is greatest, or it may be referred to the peripheral distribution 
of the involved intercostal nerves (anterior aspect of the lower thorax or 
the upper abdomen). Physical examination discloses restriction of the 
movements of the chest on the affected side and the pathognomonic 
friction sound. This is a jerky or interrupted, rubbing, rasping, creak- 
ing, or new-leather sound, audible most commonly during inspiration, 
especially at the end of inspiration, but sometimes during inspiration 
and expiration (to-and-fro sound); it seems to be near the auscultating 
ear, superficial, and it may be increased in intensity by pressure, as by 
the stethoscope; it often disappears temporarily after the patient has 
taken several deep inspirations (smoothing of the rough and irregular 
pleural surface?); and it is not always audible at the site of the pain 
(but rather laterally). Occasionally the frictions may be palpable. The 
breath sounds are usually feeble, from restriction of the movements of 
the chest. 



566 DISEASES OF THE PLEURA 

Diagnosis. — The "stitch in the side" and the pleural frictions make 
the diagnosis unmistakable. In intercostal neuralgia there are points 
of tenderness along the course of the intercostal nerves, and an absence 
of fever and of pleural frictions. In pleurodynia also there is an absence 
of fever and of pleural frictions. 

Prognosis. — Inasmuch as dry pleurisy is rarely a primary disorder, 
the prognosis is that of the attendant condition. The pleural manifes- 
tations, as a rule, subside spontaneously; but it is important to bear in 
mind that dry pleurisy may be merely the beginning of serofibrinous 
pleurisy. 

Treatment. — In addition to attention to the primary disorder, the 
treatment should consist of counterirritation (iodine, blisters, or a 
mixture of equal parts of menthol, camphor, and chloral), opium or 
morphine if the pain is very severe, and other measures to be mentioned 
presently under serofibrinous pleuritis. 



SEROFIBRINOUS PLEURITIS. 

(Pleurisy with Effusion.) 

Etiology. — There is no sharp line of demarcation between fibrinous 
and serofibrinous pleuritis; they represent different stages of the one 
process — alike etiologically (bacteriologically) and pathologically. Pleu- 
risy with effusion, however, is most common in young male adults, 
apparently previously healthy; it is often believed to be a primary 
disorder, developing after exposure, an alcoholic debauch, etc. But 
these act likely merely as predisposing factors, since there is good 
evidence that at least 75 per cent, of so-called primary or cryptogenetic 
pleuritides are tuberculous in origin, the source of infection usually 
being calcified or fibroid bronchial lymph nodes (more or less quiescent 
tuberculosis). In children most cases of pleuritis follow pneumonia. 

Pathology. — As a rule, the disease is unilateral, slightly more common 
on the right side than on the left. In the early stages the lesions are 
identical with those of fibrinous (dry) pleurisy. Soon, or in some cases 
from the beginning, a more or less abundant fluid exudate is poured out — 
thin, serous, alkaline, yellowish, albuminous (3 to 7 per cent.), usually 
at least slightly turbid, and often containing fibrinous flocculi; in some 
cases the fluid has a greenish tint; or it may be purulent or hemorrhagic 
(purulent and hemorrhagic pleuritis). The fluid varies in amount up 
to 3 to 5 liters; and it may be entirely free, or more or less encapsu- 
lated — in a single or a multilocular enclosure. Special localization of the 
lesions warrants the terms pericarditic pleuritis, mediastinal pleuritis, 
diaphragmatic pleuritis, interlobar pleuritis, etc. The presence of a 
large amount of fluid leads to distention of the affected side of the chest, 
and to compression and displacement of adjacent organs — the lungs, 
the mediastinum, the heart, the diaphragm, the liver, the spleen, etc. 
As a rule, the fluid is absorbed spontaneously or it is removed by thora- 



Serofibrinous pleUritis 567 

centesis; following which the opposed surfaces of the pleurae become 
adherent and ultimately, through organization, permanently united, 
leading to obliteration of the pleural sac. The new fibrous tissue 
contracts and gives rise to more or less distortion of the affected side 
of the chest, retraction of the ribs, narrowing of the intercostal spaces, 
scoliosis (convexity toward the healthy side), displacement of adjacent 
organs, especially the heart (retraction toward the affected side). In 
the course of time these may be almost if not quite completely overcome, 
especially if not marked originally; in other cases the pleural adhesions 
may become extraordinarily thickened and effectually prevent normal 
expansion of the lung, or sending prolongations into the lungs they may 
lead to a form of chronic interstitial pneumonitis. The other lung in 
these circumstances becomes the seat of so-called compensatory emphy- 
sema and the corresponding side of the chest becomes notably enlarged. 

Symptoms. — The onset of the disease may be frank or insidious. In 
some cases the symptoms are not distinctive, scarcely even suggestive, and 
the disorder is disclosed only by physical examination (latent pleurisy). 
In other cases there is a gradual onset, with symptoms referable to the 
chest. In still other cases the onset is more or less abrupt, and attended 
by pain in the side, cough, and fever, as in acute fibrinous pleurisy; 
not infrequently there is a chill, or chilliness, which may last some 
hours or recur, and there are usually such general manifestations of 
infection and toxemia as headache, malaise, anorexia, etc. The pain 
is often extremely severe, stabbing in character, and localized to the 
side or the peripheral distribution of the involved intercostal nerves, 
although it may radiate to the abdomen, the opposite side, etc.; it is 
aggravated by cough, breathing, pressure, and change of posture. The 
cough is usually hard and dry; occasionally there is slight mucous expecto- 
ration. The breathing is usually rapid and superficial, less from dyspnoea 
per se than from pain set up by deep inspirations. The fever is variable, 
and rarely exceeds 101° to 102°; at the end of a week or ten days, as a 
rule, there is some evidence of lytic decrease of the temperature, but 
slight fever may continue for several additional weeks, and exacerba- 
tions from time to time are not uncommon. In unusual cases there 
may be no fever (probably, however, some fever, if sufficiently often 
searched for). As the serous exudate is poured out, and the inflamed and 
sensitive pleural surfaces are separated (the fourth to seventh day, as a 
rule), the pain and cough lessen and may disappear altogether; but 
should the amount of fluid be considerable, 200 c.c. in a child, 800 c.c. 
or more in an adult, symptoms due to the presence of the fluid as such 
and to the consequent compression and displacement of adjacent viscera 
develop. These comprise especially dyspnoea, cyanosis, and frequency 
and smallness of the pulse, which may or may not be present when the 
patient is quiet, but assuredly develop upon exertion. 

Physical Signs. — Pleurisy may be suggested by an initial "stitch in the 
side" and fever, but the diagnosis, especially of effusion, is impossible 
in the absence of a physical examination. In the early (dry) stage the 



568 DISEASES OF THE PLEURA 

patient is likely to lie on the healthy side to avoid increasing pain by 
pressure on the affected side, but when the effusion becomes large he is 
likely to lie on the diseased side, so as to allow free and unrestricted 
expansion of the unaffected side; but he may lie on his back or sit semi- 
erect in bed. When effusion has occurred the affected side is usually 
enlarged visibly and measurably (normally the right semicircumference 
is about 2 cm. greater than the left); the interspaces are on a level with 
the ribs or bulging. The respiratory movements of the chest and dia- 
phragm on the affected side are lessened or abolished, the functional 
incapacity of the diaphragm showing well in the absence of Litten's 
sign and upon fluoroscopic examination. In typical cases (there are 
many atypical cases) directly over the fluid there are dulness on percus- 
sion, increased resistance, diminished or absent tactile and vocal fremitus, 
and weak or absent breath sounds; the higher the upper limit of fluid 
(the greater the amount, as a rule) the more marked are these signs, 
and they increase in intensity from above downward. The tactile and 
vocal fremitus (normally more marked at the right apex and often 
throughout the right lung) may be normal above the fluid in moderate- 
sized effusions; generally they are increased directly above the fluid 
(at the upper limit of dulness) and toward the vertebras on account of 
compression of the lung; they may be well marked or increased also in 
the event of adhesions binding the lung to the chest wall, and apparently 
in children from unknown causes (perhaps small chests and considerable 
elastic intrapleural tension). 

The upper limit of the dulness varies with the height of the fluid (which 
may or may not be proportionate to the amount), but it does not directly 
indicate the level of the fluid, since fibrinous exudate and compressed 
lung above the fluid also cause dulness. In small and moderate effusions 
the upper limit of the fluid (and of the dulness) varies, being influenced 
by intrapleural capillarity, retraction of the lung, and the position of the 
patient during the development of the fluid. Small effusions (less than 
500 c.c.) may cause a small area of dulness posteriorly near the angle 
of the scapula, in the axilla, in Traube's semilunar space, or in the 
cardiohepatic (Ebstein's) angle. A significant feature of the upper 
limit of moderate effusions is their irregular outline; often this is low near 
the vertebras, rises near the posterior or the midaxillary line, and falls 
again in front (the S-shaped curve of Ellis and Garland), due in part to 
intrapleural capillarity and the lateral-prone posture of the patient, espe- 
cially during the period of development of the fluid. Had the patient been 
erect, the upper limit of dulness is more likely to be nearly horizontal. 
In very large effusions the dulness may extend up to or above the third 
rib in front and the spine of the scapula posteriorly. In perhaps the 
majority of cases (despite prevailing opinions to the contrary), the upper 
limit of dulness does not change with change in the posture of the 
patient, because the apposed surfaces of the pleurae are usually adherent 
just above the fluid,; in the less common cases (few limiting adhesions) 
postural change in the dulness may occur after a short time and after 



SEROFIBRINOUS PLEURITIS 569 

a number of deep inspirations. There is no respiratory change in the 
upper limit of dulness. Above the dulness there is usually a vesiculo- 
tympanitic note (Skodaic resonance), due to relaxation o the lung; 
or the note may be normal. The common vesiculotympanitic note 
near the vertebrae, in the depression of the S-shaped curve of Ellis-Gar- 
land, may be accentuated and increased in large effusions by unusual 
compression of the lung. A triangular area of dulness along the ver- 
tebrae on the side opposite the effusion may be observed in moderate or 
large effusions (Koranyi-Grocco triangle), and is due to displacement 
and compression of the mediastinum by the expanding pleural sac and 
removal of the resonant lung from the neighborhood of the vertebrae. 
Williams' tracheal tone and the so-called cracked-pot sound may some- 
times be elicited in the first and second intercostal spaces in the event 
of considerable lung compression. Percussion, as well as palpation, 
also discloses displacement of the adjacent organs, notably the heart 
and the liver, less frequently the spleen and the stomach. The displace- 
ment of the heart may be extreme, but torsion does not occur, and the 
pulsation sometimes observed far to the right in left-sided effusions 
must not be interpreted as the apex beat. The lower border of the 
liver may reach to the umbilicus or beyond in large right-sided effusions. 
The lung on the unaffected side is commonly hyperresonant from 
compensatory inflation; it may encroach upon the normal dulness of the 
heart, liver, or spleen; but on the left side (in right-sided effusion) heavy 
percussion may bring out a tympanitic note from the stomach and 
intestines, especially if they be distended. 

The weak or absent breath sounds usually heard over the fluid (or 
dull area) may be modified by attending circumstances. As a rule, 
in moderate or large effusions, the breath sounds decrease in intensity 
from above downward, and low down are totally inaudible; but at the 
upper level of the dulness, bronchovesicular or bronchial breathing 
is common from compression of the lung and non-activity of the alveoli; 
in very large effusions this bronchial breathing may be audible only 
below the clavicle and in the supraspinous fossa, or no breath sounds 
may be audible. In some cases breath sounds, usually more or less 
feeble bronchial breathing, may be heard directly over the dull area. 
This is due in some cases to the layer of fluid being thin (less than 2 cm.), 
to adhesions binding the lung here and there to the costal pleura, and 
to conditions favoring conduction (perhaps related to intrapleural 
tension). The last mentioned seem to be especially operative in children 
in whom the breath sounds in pleural effusion are often quite as loud 
and bronchial in character as they are in pneumonia; and they may be 
associated with bronchophony. Egophony is sometimes present, usually 
over the upper half or third of moderate-sized effusions. The whispered 
voice (pectoriloquy) is said to be transmitted (direct auscultation) 
through a serous, but not through a purulent effusion (BaccehTs sign). 
Pleural frictions are commonly audible at the upper limit of dulness; 
and moderately loud consonating rales are rarely audible over the dull 



570 DISEASES OF THE PLEURA 

area in the event of the breath sounds also being audible. A systolic 
murmur may develop toward the base of the heart, being due to 
anemia, fever, or pressure on, or torsion of, the great vessels. Usually 
there is a slight leukocytosis — 10,000 to 15,000. 

Diagnosis. — The diagnosis of pleural effusion is dependent wholly 
upon the physical signs, of which the following are the most important: 
Unilateral increase in the size of the chest, immobility during respiration, 
diminished or absent tactile fremitus, dulness on percussion, and displace- 
ment of the adjacent viscera (heart, mediastinum, liver, etc.). Pneu- 
monia (sometimes suggested by bronchial breathing, bronchophony, 
etc.) may be excluded by the absence of the characteristic mode of onset 
of pneumonia (initial chill, high fever, dyspnoea, and rusty expectora- 
tion), and by the more marked dulness and greater resistance, absence 
of tactile fremitus, and the displacement of adjacent viscera that occur 
in pleural effusion. Temporary absence of tactile fremitus and of 
bronchial breathing sometimes occur in pneumonia, being due to plug- 
ging of a large bronchus, but coughing usually dislodges the obturating 
plug of mucus and fibrin, and tends immediately to clear the diagnosis. 
In the event of doubt, and with a view to determine the nature of the 
pleurisy, resort may be had to exploratory puncture and the removal 
of a small amount of fluid. Hydrothorax may be excluded by the ab- 
sence of its special etiological factors (cardiac and renal disease, advanced 
cachectic states, etc.), by the free mobility of the fluid (which is not 
confined by adhesions), and by examination of some of the fluid removed 
by an exploratory needle. Pulmonary and pleural tumors, which may 
be attended with pleural fluid, may cause diagnostic embarrassment, 
but they give rise to irregular dulness, the general evidences of tumors 
(anemia, cachexia, etc.), to obvious local growth or metastasis (medias- 
tinum, cervical glands, etc.), and often to a hemorrhagic, sometimes chyli- 
form fluid, in which particles of the tumor or tumor cells may be found. 
A pericardial effusion may be excluded by the preponderance of physical 
signs posteriorly rather than anteriorly, the absence of the especially 
significant physical signs of pericardial fluid, the presence of a displaced 
rather than an obscured heart, and the less-marked evidences of cardiac 
embarrassment (dyspnoea, cyanosis, feeble heart sounds, weak pulse, 
etc.). 

Situation of the Exudate. — The foregoing description applies 
to the majority of cases, in which the fluid involves more or less of the 
pleural sac, and extends from below upward. In other cases the 
lesions are distinctly circumscribed and the fluid sacculated. This 
may occur anywhere, but especially anteriorly and in the axilla; it gives 
rise to the physical signs (already mentioned) over a restricted area 
Diaphragmatic pleurisy gives rise to pain and tenderness in the epi- 
gastrium (especially at the xyphoid), which may radiate to the back; 
often it is very severe and simulates angina pectoris. There is often 
distressing hiccough and spasm of the upper part of the rectus muscle; 
perhaps marked dyspnoea and dysphagia. The fluid accumulating 



SEROFIBRINOUS PLEURIT1S 571 

between the diaphragm and the diaphragmatic surface of the lung 
may not cause noteworthy dulness, but only the signs of local compres- 
sion of the lung and displacement of the adjacent viscera. The fluid 
may be recognized by radiographic examination. Interlobar pleurisy 
(usually postpneumonic and suppurative) may be detected by an area 
of dulness corresponding to the fissure between the lobes, radiographic 
examination, and in most cases the symptoms of lung abscess or 
empyema. 

Nature of the Pleuritis. — The nature of the pleurisy may be 
recognized by a chemical, microscopic, cytological, and bacteriological 
examination of the fluid. The fluid, as a rule, is pale amber in color, 
slightly cloudy, alkaline, has a specific gravity of 1015 to 1024, contains 
3 to 7 per cent, of albumin, and it usually clots after removal. It con- 
tains usually a few erythrocytes and leukocytes, and endothelial cells 
(mostly fatty) in varying proportion. Cytologically preponderance of 
lymphocytes is indicative of the tuberculous nature of the pleuritis; 
preponderance of leukocytes, of pyogenic infections; and preponderance 
of endothelial cells, of mere transudation or malignancy. The tuberculous 
nature of the process may be further determined by obvious involvement 
of a lung or another serous membrane, by a positive response of the 
patient to a tuberculin test, and by inoculating lower animals with some 
of the fluid; later this becomes apparent in about one-third of the cases 
by the patient developing tuberculosis. 

Prognosis. — In uncomplicated cases the immediate prognosis is good, 
since the general tendency of the disease, despite the common tuber- 
culous origin, is toward recovery. The usual duration is from three to 
six or eight weeks. The fever, as a rule, subsides at the end of ten days 
or two weeks, but recurrences and exacerbations are not uncommon. 
With the decline of the fever the fluid tends to become absorbed (appar- 
ent in lessening of the physical signs of fluid and the development of 
redux crepitation). This may occur very slowly, and it may not occur 
at all, although resorption may occur even after months ; recurrence after 
removal is common. Following absorption or removal of the fluid, 
the pleural sac, in whole or in part, becomes obliterated by fibrous 
adhesions; these, if thin and non-indurative, are well borne, but if thick 
and cicatricial they lead to induration of the lung, distortion of the 
chest, and displacement of the adjacent viscera, which, together with the 
later possibility of the development of pulmonary tuberculosis, renders 
the ultimate prognosis doubtful. Sudden death sometimes occurs from 
syncope following exertion, myocardial degeneration, mechanical 
embarrassment of the circulation from displacement of the heart and 
pressure on or torsion of the vessels, pulmonary embolism, thrombosis, 
or oedema; or it may follow sudden withdrawal of a large amount of 
fluid. 

Treatment. — The patient should be confined to bed in a well-venti- 
lated room or out-doors, and placed on a liquid or semisolid, easily 
digestible diet. The bowels should be thoroughly evacuated (calomel 



572 DISEASES OF THE PLEURA 

or blue mass and a saline cathartic), and they should be kept freely 
open throughout the continuance of the disease. In the early stage 
pain usually demands relief, and it should be relieved — by an ice bag, 
dry cups, or strapping the side (as in fracture of the ribs); or a hypo- 
dermic injection of morphine may be given (it should not be withheld 
when needed) ; or one may use repeated small doses of powdered opium 
or extract of opium in a pill during the day, and, if needed, in addition 
administer a Dover's powder in the evening. The use of opium is 
sanctioned by long usage; it not only relieves the pain and the distress 
of breathing, but it is also believed to exercise a favorable, so-called 
antiphlogistic action on the capillary circulation of the pleura (and 
other serous membranes), and thus to control the inflammatory phe- 
nomena. Small doses of quinine as recommended in pneumonia, seem 
to be a useful addition. In some cases, of supposed rheumatic origin, 
salicyl preparations (salicylic acid and its salts, salol, salicin, aspirin, 
etc.) appear to do good; at all events, in sufficient dosage they tend to 
relieve pain. During the early fever days of the disorder the comfort 
of the patient may be promoted by simple febrifuge mixtures (potassium 
citrate, spirit of nitrous ether, solution of ammonium acetate, etc.). 

When the stage of effusion has been reached one may await the 
spontaneous absorption of the fluid, attempt to hasten its absorption 
by medicinal means, or remove the fluid by thoracentesis. In general 
there is a tendency toward the spontaneous absorption of the fluid; but 
this often requires considerable time : it may not occur for months, and 
it may not occur at all. Attempts to hasten the absorption of the fluid 
are sometimes made — by counterirritation (iodine and blisters locally, 
and the iodides internally); by using a dry diet (very little fluid at or 
between the meals) and provoking copious bowel movements (concen- 
trated saline cathartics in the morning before breakfast) — so-called Hays' 
method; and by the use of a chloride-poor diet. More or less satisfac- 
tory results sometimes attend these measures, but, as a rule, they are 
disappointing. 

The most efficacious treatment consists in withdrawal of the fluid 
by thoracentesis. In moderate-sized and large effusions this may be 
done at any time with good results; but it is especially indicated as 
soon as the fluid appears to be not increasing in amount. This may 
be as early as the tenth day or thereabout, and at a time when the patient 
still has fever and few if any subjective pressure symptoms; but early 
withdrawal of the fluid is indicated because it hastens convalescence; 
because it relieves the compressed lung and displaced and embarrassed 
heart and bloodvessels, and in consequence permits of the early resump- 
tion of full functional activity; and because it obviates the danger of 
sudden death which occasionally occurs from high intrathoracic press- 
ure. In the event of delaying thoracentesis, there are certain positive 
indications for withdrawing the fluid that should never be ignored; 
thus, aspiration is indicated in all cases in which there is marked dis- 
placement of the heart, and immediately upon the occurrence of embar- 



SEROFIBRINOUS PLEURITIS 573 

rassed cardiac action (rapidity, irregularity, the development of a mur- 
mur), dyspnoea, cyanosis, or syncope; in unilateral effusion, when the 
dulness extends to the second interspace, or if the dulness does not 
extend so high, upon the development of physical signs of fluid accumu- 
lating in the other side; in bilateral effusions when both sides are half 
full (dulness posteriorly to the middle of the scapula); and when there 
is no evidence of absorption of the fluid after a week or ten days of 
normal temperature. 

The preferable site for introducing the aspirating needle is the 
eighth intercostal space just external to the angle of the scapula; 
some physicians prefer the seventh interspace in the midaxillary line. 
The needle should be introduced close to the upper margin of the rib 
so as to avoid wounding the intercostal artery. The fluid should be 
withdrawn very slowly; the amount withdrawn should depend, of 
course, upon the amount present, but also on the reaction of the patient. 
Very slow withdrawal will permit the withdrawal of considerable fluid, 
but it is rarely necessary or desirable to remove more than 1000 to 
1500 c.c; the removal of a relatively or actually small amount is often 
followed by spontaneous absorption of the remainder. The operation 
should be discontinued when the pulmonary pleura is found to impinge 
against the aspirating needle inserted only a short distance, and when 
the patient complains of a short, hacking, paroxysmal cough (the 
usual signal for discontinuance), pain, or syncope. A second aspira- 
tion, rarely a third, may be required. Continuous drainage is prefer- 
able to repeated operations in recurrent cases. Barr has suggested the 
introduction into the pleural sac, during and after the withdrawal of 
the fluid, of a volume of air equal to one-half or three-fourths of that 
of the fluid removed, to obviate the development of a negative intra- 
plueral pressure and to permit gradual expansion of the compressed 
lung; and also the introduction of one dram (4 c.c.) of adrenalin chloride 
(1 to 1C00), to contract the bloodvessels and lessen secretion. Others 
have suggested the injection of gases, notably nitrogen. 

Thoracentesis is occasionally attended by more or less serious unto- 
ward consequences, such as wounds of the intercostal artery, the lung, 
the liver, the heart, or the spleen; pulmonary oedema (albuminous ex- 
pectoration), which is usually due to the too rapid withdrawal of the 
fluid (it should be treated with morphine and atropine hypodermicly) ; 
pneumothorax, hemothorax, subcutaneous emphysema, syncope (cere- 
bral anemia), sudden death from pulmonary or cerebral embolism, etc. 

The patient's strength must be conserved throughout the course of the 
disease, especially during convalescence, by the use of tonics, such as 
iron, quinine, strychnine, cod-liver oil, the hypophosphites, etc., good 
food, and fresh air. Should the lung not be speedily restored to good 
function, pulmonary exercises designed to inflate the lung, such as 
repeated deep inspirations several times daily, or the blowing of water 
through a narrow tube from one large flask to another, should be re- 
sorted to. 



574 DISEASES OF THE PLEURA 

PURULENT PLEURITIS. 

(Suppurative Pleurisy; Empyema.) 

Etiology. — Purulent pleuritis is usually a secondary process caused by 
the pneumococcus, the streptococcus, or the staphylococcus, rarely per- 
haps to the tubercle bacillus, the colon bacillus, the typhoid bacillus, etc. 
In some cases the disorder begins as a serofibrinous pleuritis and is set up 
by the usual etiological (bacterial) factors of this form of pleuritis; some 
serofibrinous exudations, perhaps originally more opaque and cell-rich 
than is the rule, become still more opaque and cell-rich, that is, sero- 
purulent, even distinctly purulent (the last mentioned usually the result of 
secondary infection set up perhaps by thoracentesis, or other factors). 
In other cases the process is purulent from the beginning or speedily 
becomes purulent. In children the pneumococcus is the common cause, 
most of the cases following pneumonia (metapneumonic form). In 
adults streptococci and staphylococci are the more frequent causes, 
but pneumococcic forms also occur. The common antecedent disorders 
are: Tuberculous pulmonary cavities ruptured into the pleura (the 
empyema in these cases being a mixed and not a pure tuberculous 
infection); tuberculosis, suppurative and traumatic disease of adjacent 
tissues — such as the mediastinum, the bony framework of the chest, 
the abdominal organs, etc. (lymphogenic infection); and distant local- 
ized infections (septicopyemia), or general infections (scarlatina, measles, 
dysentery, typhoid fever, etc.), in which secondary pyogenic infections 
are rather common. 

Pathology. — In cases with less pus and more serum the changes in the 
pleura are quite like those of serofibrinous pleuritis, although more 
marked; the pleura is thickened and covered with a thick fibrinopuru- 
lent exudate; and there is marked polynuclear leukocytic infiltration; 
the fluid is more opaque and contains more cells. In cases frankly 
purulent the fluid usually separates into a heavy corpuscular lower 
layer exhibiting the ordinary characteristics of pus, and a lighter upper 
serous layer, greenish yellow in color. In the pneumococcic cases, 
especially in children, the exudate is likely to be thick and creamy and 
to have a sweetish disagreeable odor; in the streptococcic and staphylo- 
coccic cases the fluid usually is thinner. The fluid may become fetid 
(fetid or putrid pleurisy), especially in cases following stab wounds 
of the chest, abscess or gangrene of the lung, carcinoma of the oesophagus, 
appendicitis, etc. 

Symptoms. — In some cases the onset and the course of the disease for 
some time are identical with those of serofibrinous pleuritis, of which 
purulent pleuritis may be only an advanced stage. In other cases 
following antecedent symptoms of the primary disorder, the develop- 
ment of the pleuritis may be abrupt, with a chill, high temperature, 
severe pain in the side, and general evidences of toxemia. In many 
cases the suppurative character of the exudate is not suspected for 



PURULENT PLEURITIS 575 

some time, unless the disease develops into a frank case of septicopyemia. 
Long continuance of fever otherwise unexplained, however, suggests 
the suppuration, as do also progressive pallor, weakness, and loss of 
flesh; this is rendered more certain by the occurrence of paroxysms of 
chills (or chilliness), fever, sweats, and augmented polynuclear leuko- 
cytosis. 

Physical Signs. — The physical signs in general are identical with those 
of serofibrinous pleuritis, that is, the physical signs no not disclose the 
character of the exudation. However, in purulent pleuritis the inter- 
costal spaces are more likely to be bulging than in serofibrinous pleuritis 
on account of paresis (seropurulent infiltration) of the intercostal 
muscles; in children there may be an extraordinary enlargement of the 
affected side of the chest; whispered pectoriloquy is less well transmitted 
through a purulent than through a serous exudation (Baccelli's sign); 
and a localized area of oedema may develop over the fluid — which is 
almost if not quite pathognomonic of the purulent character of a pleural 
exudate. In exceptional cases the purulent exudate (very rarely also a 
serofibrinous exudate) transmits a cardiac systolic pulsation to the 
chest wall (pulsating empyema) between the second and fourth ribs 
anteriorly, or the third and fifth ribs in the axilla, or over a very wide 
area. The cause of this is not definitely known, but important factors 
seem to be left-sided pleural exudation (it is very rare in right-sided 
effusions), a large amount of fluid, paresis (relaxation, due to cedema- 
tous infiltration) of the intercostal muscles, and forcible action of the 
heart. Some observers believe the pulsation to be transmitted from the 
aorta rather than from the heart. This swelling may rupture through 
the costal pleura and form a pulsating mass directly beneath the skin 
(empyema necessitatis), and it may rupture externally — usually toward 
the lower part of the thorax or near the sternum; or by gravitation 
the empyema may reach even as low as the groin; or it may rupture 
into the lung and be evacuated through a bronchus, the trachea, and 
the mouth, or into the oesophagus, the stomach, etc. 

Diagnosis. — The physical signs so essential in the diagnosis of any 
pleural effusion do not determine the character of the fluid; but long- 
continued fever, local oedema of the chest wall, and recurring chills, 
fever, sweats, and polynuclear leukocytosis constitute conclusive evi- 
dence of the purulent character of the fluid. In any case of doubt 
recourse should be had to the exploring needle, and a small amount 
of fluid should be removed and examined bacteriologically and cyto- 
logically. In many cases the amount of fluid (pus) is small and dis- 
tinctly localized — to the base, between the lobes, etc., and being detected 
serves to explain ill-understood fever states (delayed convalescence 
from pneumonia, inexplicable attacks of fever after scarlatina, typhoid 
fever, etc.). It is scarcely likely that a pulsating empyema will be 
mistaken for an aneurysm. 

Prognosis. — Purulent pleuritis not properly treated is a chronic 
disorder tending ultimately to death. Sometimes the cases that per- 



576 DISEASES OF THE PLEURA 

forate spontaneously or through the lung end in recovery, the fistulous 
tract finally healing; or the fistula may persist with more or less dis- 
comfort to the patient and perhaps eventual amyloidosis, etc. The 
prognosis is better in children than in adults, especially under appro- 
priate treatment. Marked retraction and deformity of the chest usually 
follow in the event of recovery. 

Treatment. — Purulent pleuritis is essentially a surgical disorder, and 
should be treated on surgical principles; as an abscess anywhere in the 
body, so should an empyema be promptly evacuated upon discovery 
and thoroughly drained. Preliminary aspiration is not necessary, 
unless with a view to relieve pressure pending more thorough evacua- 
tion. The basis of successful treatment is free drainage, which sometimes 
may be achieved by simple free incision, especially in children; in 
other cases it may be necessary to resect one or more ribs. Irrigation 
of the cavity is sometimes resorted to in cases of putrid pleuritis, but 
otherwise is not necessary. Following evacuation of the pus, persistent 
efforts must be made to cause expansion of the compressed lung — by 
calisthenic exercises, pulmonary gymnastics, blowing water through 
a narrow tube from one bottle to another, etc. Mutilating (Estlander) 
operations, comprising resection of several ribs, are sometimes necessary 
finally to close the cavity. 



HEMORRHAGIC PLEURITIS. 

Etiology —In virtually all cases of serofibrinous pleuritis the fluid 
exudate contains a variable number of erythrocytes. Usually these 
pass unnoticed unless the fluid is examined microscopically; sometimes, 
however, the erythrocytes are in such excessive numbers as to give a 
more or less well-marked hemorrhagic tint to the fluid. This occurs in 
certain cases of the so-called primary or idiopathic pleuritis which on 
careful study are found to be tuberculous, as well as the more frankly 
tuberculous cases with the eruption of miliary tubercles (rupture of 
new-formed capillaries) ; in primary and secondary tumors of the pleura ; 
in the pleurisy of asthenic and cachectic states, such as chronic nephritis, 
cirrhosis of the liver, purpura, scurvy, leukemia, and other blood dyspa- 
sias, etc. (in which cases it is not always a true inflammation). 

Pathology. — The lesions vary with the causative factors (tuberculosis, 
tumors, etc.). In many cases they are quite like those of the analogous 
serofibrinous pleuritis — with the addition of some blood to the exudate. 
In cachectic states the pleura often shows hemorrhagic foci (usually 
petechial). 

Symptoms. — The symptoms are usually those of serofibrinous pleuritis, 
from which hemorrhagic pleuritis is not to be distinguished except by 
examination of the fluid. In other cases the symptoms are those of tumor 
of the lung or pleura, to which the physical signs of fluid in the chest 
become superadded. In other cases (blood dyscrasias, asthenic states) 



CHRONIC PLEURITIS 577 

the phenomena are analogous to those of hydrothorax, and are disclosed 
usually only by a physical examination of the chest. 

Diagnosis. — The diagnosis is dependent upon the physical signs of 
fluid in the pleura and an examination of the fluid; its hemorrhagic 
character can at most be merely suspected before some of the fluid is 
withdrawn. The condition should be distinguished from hemothorax 
(hemorrhage into the pleural sac), which may result from traumatism 
and injury to the chest wall or the thoracic organs, puncture of an 
intercostal vessel during aspiration, rupture of an aneurysm, ulcerative 
processes involving the pleurae and pulmonary vessels, etc. ; the symptoms 
are the general manifestations of more or less rapid bleeding and the 
physical signs of the more or less rapid accumulation of fluid in the 
pleura. 

Treatment. — The treatment of hemorrhagic pleuritis, in so far as it 
differs from that of serofibrinous pleuritis, is dependent solely upon the 
associated conditions and causative factors. 



CHRONIC PLEURITIS. 

(Chronic Pleurisy with Effusion; Chronic Adhesive Pleurisy.) 

Two types of chronic pleuritis may be distinguished — the one with, 
the other without, a fluid exudation. 

Chronic Pleuritis with Effusion.— This may develop insidiously, 
or it may follow acute serofibrinous pleuritis: the etiological factors, 
the lesions, and the symptoms may be quite like those of the acute pro- 
cess. Rarely the fluid persists, little if at all changed, for months, without 
occasioning noteworthy symptoms; often, however, there is dyspnoea, 
especially on exertion. The physical signs, the diagnostic criteria, and 
the treatment, are quite like those of serofibrinous pleuritis. 

Chronic Adhesive Pleuritis. — Etiology. — Chronic pleural adhesions 
are encountered under varying circumstances: (1) They may represent 
a primary chronic, originally fibrinous pleuritis — which perhaps may 
develop abruptly, but more commonly comes on insidiously; the organi- 
zation of the fibrinous exudation leads to adhesion of the apposed 
layers of the pleura and more or less widespread obliteration of the 
pleura sac. These are the adhesions so commonly encountered at 
necropsies, often in subjects who during life presented no noteworthy 
evidences of their presence; originally inflammatory in nature, they are 
later analogous to scar tissue formation elsewhere in the body. (2) 
Chronic pleural adhesions are also the evidences of postserofibrinous 
and purulent pleuritis; they represent the process of healing, of scar 
formation. Following absorption of the fluid exudation, the apposed 
layers become adherent, and the sequential process of organization and 
cicatrization lead to their permanent union. As a cicatrix elsewhere, 
the new-formed fibrous tissue undergoes more or less contraction, and, 
especially in cases of empyema, may lead to extraordinary retraction and 
37 



578 DISEASES OF THE PLEURA 

deformity of the chest, displacement of the intrathoracic organs, and 
fibrous connective tissue overgrowth in the lung (chronic interstitial 
pneumonitis, bronchiectasis, etc.). The process is usually most marked 
at the base, where the two layers of the pleura usually become inseparable 
and indistinguishable, and represented by thick fibrous connective tissue. 
(3) Chronic adhesive pleuritis may be definitely tuberculous; that is, 
both layers may be adherent, more or less, often considerably, thickened 
(to 5 mm. or more), and the seat of large caseous tubercles, as well as of 
small miliary and fibroid tubercles; the lesions may involve one or both 
pleura, perhaps also the pericardium, and give rise to veritable tumor 
masses. (4) Chronic adhesive pleuritis may be part of a general serositis 
(multiple serositis, polyorrhomenitis), in which the pleurae, pericardium, 
and peritoneum become involved in varying combinations; the serous 
membrane becomes thickened and hyaline and much resembles con- 
fectioner's sugar-icing (Zuckerguss — whence the Zuckerguss-leber, -milz, 
-herz, -lunge, etc., of the Germans). The pleura and the other serous 
sacs may be totally or partially obliterated, and if partially only, there 
may or may not be also some fluid. 

Symptoms. — The symptoms vary. In some cases there may be a 
dragging pain or general aching in the side, aggravated by overexertion 
or inclement weather; sometimes even a sharp pain occurs. Often 
there is more or less dyspnoea, especially on exertion; and there may be 
other symptoms due to associated conditions, such as cough and expecto- 
ration in chronic bronchitis, general evidences of tuberculosis, and 
symptoms referable to other serous membranes. 

Physical Signs. — The physical signs vary with the extent of the ad- 
hesions and the degree of contraction. In mild cases there is more or 
less restriction of the respiratory movement of the affected side of the 
chest and feeble breath sounds. In more marked cases, the affected 
side is definitely contracted and more or less immobile, especially at the 
base; the other side may be distended and the seat of exaggerated 
compensatory respiratory movements; the tactile and vocal fremitus 
and the breath sounds are lessened in intensity and may be absent; the 
percussion note is impaired and may be quite dull; there is no respiratory 
movement of the percussion resonance at the edges of the lung with the 
phases of respiration; and Litten's sign is absent. Auscultation some- 
times reveals peculiar, dry-leathery, so-called friction sounds. In 
advanced cases the thorax may be extraordinarily deformed, the ribs 
retracted and approximated, the shoulder lowered, the vertebrae curved 
(the concavity toward the affected side); etc.; the heart may be 
uncovered by the lung, and it, as well as the liver, spleen, etc., may be 
more or less displaced. 

Diagnosis. — The diagnosis depends upon the past history of the patient, 
the immobility and retraction of the chest, and the impaired resonance, 
feeble breath sounds, and other physical signs of a thickened pleura 
interposed between the lung and the chest wall. 



HYDROTHORAX 579 

Prognosis. — The prognosis varies with the severity and extent of the 
adhesions and the presence or absence of complicating conditions, such 
as fibrosis of the lung, bronchiectasis, deformity of the thorax, etc. 

Treatment. — Attention to the general health of the patient is of prime 
importance. The hygienic conditions must be the best attainable, and 
the food must be of the best quality and generous in amount. If fluid 
is present in the pleura it should be removed by aspiration. Regulated 
exercise and pulmonary gymnastics are of marked service in favoring 
expansion of the lung in mild or moderately severe cases; but notable 
improvement can scarcely be expected when the lung is encased in a 
thick layer of cicatricial connective tissue and the thorax is markedly 
deformed. In these cases, however, if the patient lives within his reserve 
capacity, he may survive a long time in comparative comfort. Tonics 
(iron, quinine, strychnine), digestants (hydrochloric acid, tincture of 
nux vomica, etc.), and alteratives (syrup of iron iodide, cod-liver oil, 
mercury, phosphorus, etc.) are often useful adjuvants. 



HYDROTHORAX. 

(Pleural Dropsy; Pleural (Edema.) 

Etiology. — Hydrothorax, a transudation of non-inflammatory serous 
fluid into the pleural sac, is a secondary process that occurs in condi- 
tions that lead to oedema generally : disease of the heart and of the lungs 
(with consecutive cardiac failure) in consequence of passive congestion; 
and in disease of the kidneys and anemic and cachectic conditions (car- 
cinoma, sarcoma, pernicious anemia, leukemia, scurvy, etc.), in con- 
sequence of hydremia, and perhaps disease of the capillary vessels and 
toxemia. 

Pathology. — In cardiac cases, the process in the beginning at least is 
likely to be unilateral, commonly right-sided, because in addition to the 
general venous engorgement, local obstruction of the azygos veins or 
the right pulmonary veins (page 457) is added, the consequence of 
pressure by a dilated right auricle or vena cava; and when it becomes 
bilateral it is still usually most marked on the right side. In renal and 
anemic and cachectic cases it is usually bilateral. The fluid varies in 
amount from a few cubic centimeters to several liters. It is usually 
clear, pale amber in color, has a specific gravity of 1006 to 1015, and 
contains from 1 to 3 per cent, of albumin; microscopically, it contains 
a few endothelial cells, erythrocytes, and leukocytes. The pleura often 
exhibits no conspicuous changes ; but in long-standing cases a low grade 
inflammation may be set up and materially alter the appearance of the 
pleura and the character of the fluid. 

Symptoms. — The symptoms are those of the primary condition, to 
which are added the effects of pressure on the intrathoracic organs, 
dyspnoea (orthopncea), cyanosis, cough (often paroxysmal and asth- 
matic), and marked embarrasment and enfeeblement of the circulation. 



580 DISEASES OF THE PLEURA 

The physical signs are those of fluid in the chest, and are quite like 
those of serofibrinous pleuritis. The fluid, however, being thinner 
and not circumscribed by adhesions, readily shifts with change in the 
posture of the patient (pathognomonic sign of fluid). 

Diagnosis. — The diagnosis depends upon the etiological factor, the 
physical signs of fluid in the pleura, and an examination of some of the 
fluid removed. It is especially important to remember that often much 
of the distress of failing cardiac compensation is due to a right-sided 
hydro thorax that is often entirely unrecognized. 

Prognosis. — The prognosis is that of the primary disorder. 

Treatment. — The treatment is that of the primary disorder. In many 
cases of failing cardiac compensation, the greatest improvement follows 
removal of the fluid by aspiration. The condition should always be 
borne in mind and searched after, and when detected, if the patient 
does not speedily improve, the thoracentesis should be promptly per- 
formed; delay may precipitate a fatal issue, which otherwise might 
be avoided. 



PNEUMOTHORAX. 

(Pyopneumothorax; Serofibrinopneumothorax ; Hemopneumothorax .) 

Pneumothorax, the presence of air or gas in the pleural cavity, is an 
exceedingly rare disorder. The causative factors are such that an inflam- 
mation of the pleura is also induced, and inasmuch as this is usually 
purulent, the condition in the great majority of cases is pyopneumo- 
thorax; rarely the inflammatory phenomena are analogous to those 
of serofibrinous pleuritis — serofibrinopneumothorax; and still more 
rarely the exudation is hemorrhagic — hemopneumothorax. 

Etiology. — Pneumothorax (pyopneumothorax and its other modifi- 
cations) is most common in males, in adult life, and on the right side. 
It results from the access of air (which is usually infected) to the 
pleura. This may occur: (1) In perforating wounds of the chest, such 
as traumatisms (when it may be associated with subcutaneous emphy- 
sema), thoracentesis, etc. (2) In rupture of the lung, which is the 
most common cause, especially the rupture of tuberculous pulmonary 
cavities; less commonly the rupture of a pulmonary abscess and gangrene, 
bronchiectatic, bronchopneumonia and embolic cavities, echinococcus 
cyst, emphysematous bulla, etc.; or the rupture into the lung of an 
empyema, or traumatic rupture of the lung due to a fractured rib 
without laceration of the overlying skin; rarely perhaps violent mus- 
cular effort or coughing may cause rupture of a lung bound down by 
adhesions. (3) In ulcerative processes in the oesophagus, stomach, 
intestines, etc. (with perhaps a primary subphrenic abscess). (4) Rarely 
pneumothorax may arise spontaneously, in consequence of infection with 
Bacillus aerogenes capsulatus (Welch) or other gas-producing micro- 
organism. 



PNEUMOTHORAX 581 

Pathology. — The process is usually unilateral; rarely bilateral. The 
contained air may or may not be malodorous; it varies in amount up to 
2000 c.c. or more; and it is commonly associated with more or less 
seropurulent or distinctly purulent fluid and lesions similar to those of 
purulent pleuritis — all of which, soon overcoming the negative intra- 
pleural pressure of 4 to 6 mm. of mercury, causes proportionate com- 
pression and displacement of the intrathoracic and upper abdominal 
organs. In rupture of a previously healthy or an emphysematous lung- 
there may be no fluid; and in traumatic cases, as well as in cases due 
to ulcerative processes, there may be also blood — hemopneumothorax 
(or hemopyopneumothorax). The air or gas may be circumscribed or 
diffuse (circumscribed or diffuse pneumothorax). The point of rupture 
in the lung may be small or large; usually, but not always it may be 
found; it may close after permitting the access of air to the pleura. 

The following varieties of pneumothorax may be distinguished: (1) 
Open pneumothorax, in which the air enters and leaves the pleura 
during the phases of respiration; (2) closed pneumothorax, in which 
the point of rupture (usually in the lung) becomes closed, and shuts 
off from the outside air that contained in the pleural sac; and (3) 
valvular pneumothorax, which permits usually the entrance, but not 
the exit of air from the pleura; the entrance of air usually ceases 
when the intrapleural pressure is sufficient to close the opening or 
to overcome the pressure of the entering air. 

Symptoms. — Rarely, the onset is insidious, and not attended by 
noteworthy symptoms; the condition may be found accidentally by 
physical examination during life or at the necropsy. In the great 
majority of cases, however, the onset is sudden and characterized by 
severe pain in the chest, the development of (or increase of previously 
existing) dyspnoea and cyanosis, and not infrequently collapse, with 
rapid, feeble pulse, sweating, etc. 

Physical Signs. — The patient is likely to lie on the affected side, to 
permit free and unrestrained movement of the healthy lung. The affected 
side is distended, and almost if not quite immobile; the intercostal 
spaces bulge and may transmit a downy or crepitant sensation on 
palpation. The tactile fremitus is markedly diminished or absent. 
The note obtained by percussion varies, depending upon the intrapleural 
tension, the tension of the chest wall (due largely to the condition of the 
intercostal muscles), and whether the pneumothorax is of the open or 
closed variety. As a rule, the percussion note is full, clear, and hyper- 
resonant or tympanitic; it is said to have an amphoric or metallic quality 
in open pneumothorax (not a conclusive or trustworthy sign to be thus 
interpreted). Of special importance is the fact that the hyperresonant 
or tympanitic note extends far beyond the normal limits of the lung. 
Sometimes the percussion note is quite dull (said to be cases of marked 
intrapleural tension and contracted intercostal muscles). Often there 
is dulness at the base of the chest (due to concomitant fluid exudation), 
which shifts readily with change in the posture of the patient; but 



582 DISEASES OF THE PLEURA 

fluid may be present without dulness, the tympany obscuring or 
replacing the dulness. The so-called cracked-pot sound may some- 
times be elicited over an open pneumothorax. The breath sounds, as 
a rule, are much diminished or absent, especially at the lower part of 
the chest; or feeble breath sounds of a bronchial, metallic, or amphoric 
quality may be audible; or this quality may be well brought out by a 
cough. On auscultating posteriorly while an assistant with a coin taps 
another coin placed on the front of the chest, one may hear the 
so-called coin sound (bruit d'airain of Trousseau). The vocal fre- 
mitus (bronchophony) also has a metallic quality, although it is 
usually less intense than normally. Bronchial and other rales may be 
heard, and usually have a metallic quality. The metallic tinkle of 
Laennec, or falling-drop sound, may be elicited by coughing, deep 
inspiration, or change of posture; usually attributed to the falling of 
a drop of fluid or fibrin on the accumulated fluid, it is not unlikely 
due to rales produced in or about a cavity in the lung. A peculiar 
whistling sound is sometimes audible and is attributable to entrance 
or exit of air through the pulmonary opening into the pleura; this takes 
on a quite characteristic quality when the opening is below the upper 
level of the fluid. A peculiar splashing sound (Hippocratic succussion 
splash) may be heard when the patient is shaken, and is pathognomonic 
of the presence of air and fluid; it may be heard only when the 
auscultatory ear is applied to the chest, but sometimes at a distance; 
and it may be quite apparent to the patient. In addition to the fore- 
going, the physical signs of displacement of the adjacent viscera, 
especially the heart, are present; the heart sounds, although muffled, 
may have a metallic quality. 

Diagnosis. — The diagnosis, as a rule, is easy: the etiological factor, 
the mode of onset, the enlarged and immobile chest, the hyperresonant 
or tympanitic percussion note, the markedly diminished or absent 
vocal fremitus and breath sounds, the metallic quality to breath sounds 
or rales that may be audible, the coin sound, succussion splash, and 
displacement of the adjacent viscera are unmistakable. It is not likely 
that a careful observer will mistake the condition for emphysema. In 
the unusual cases in which the percussion note is dull, effusion alone 
may be suspected, but absence of the characteristic increased resist- 
ance to the percussing finger and of the other signs of pleural effusion 
should exclude error; but one must remember that fluid is usually 
associated with the air. Pulmonary cavity may be excluded by the 
absence of retraction of the chest and of sinking in of the intercostal 
spaces, and by the presence of dislocation of the heart, of the coin sound, 
of succussion splash, etc. Diaphragmatic hernia and subphrenic pyo- 
pneumothorax also must sometimes be considered in the differential 
diagnosis. Rontgen-ray examination often affords material help in the 
diagnosis. 

Prognosis. — The outlook varies with the associated conditions, but 
it is always serious. Death occurs in about three-fourths of the cases; 



CHYLOTHORAX 583 

within a short time (hours or days) in a few cases, within a few weeks 
in most of the cases (tuberculous cases). Occasionally arrest of the 
tuberculous process in the lung follows the development of the pneumo- 
thorax. Some cases become chronic and last for months or years. 
Recovery may ensue when the condition develops in a previously healthy 
subject. 

Treatment. — In some traumatic, tuberculous, and other cases the air 
becomes absorbed spontaneously; the patient, therefore, should be 
watched, kept quiet, and rendered comfortable by the use of bromides, 
morphine, and other sedatives and narcotics, if necessary; if no note- 
worthy ill consequences ensue the pneumothorax should not be mo- 
lested. Removal of the air by aspiration may lead to reopening of a 
healing point of rupture in the lung and convert a closed into an open 
pneumothorax, and induce or increase infection of the pleura. The 
cases of frank pyopneumothorax, as a rule, should be treated as are 
cases of purulent pleuritis, by incision and drainage; but one often has 
to take into consideration the general condition of the patient, the 
likelihood of the pleural fistula opening and of the disease of the lung, 
perhaps quiescent, becoming reactivated, the condition of the other 
lung, etc. The likelihood of benefit from incision and drainage are 
often almost if not quite counterbalanced by the possible ill conse- 
quences; in general, however, it is always wise to evacuate pus. In 
acute cases with marked cyanosis, orthopncea, and feeble heart action 
the pleura should be incised or aspirated without delay, and morphine 
and stimulants administered. Otherwise the treatment is that of the 
associated conditions, chiefly tuberculosis. 



CHYLOTHORAX. 

Chylothorax, the presence of a milky, opaque, and opalescent fluid 
in the pleura, may be of two types: (1) True chylothorax, in which the 
fluid is chyle. This occurs rarely in the event of obstruction or rupture 
of the thoracic duct, and still more rarely in obstruction of the sub- 
clavian vein (thrombosis, or pressure from without by tumors, etc.). 
(2) False chylothorax (pseudochylothorax), in which the fluid is chyli- 
form (adipose), the consequence of fatty degeneration of contained 
cells and of fatty (and perhaps albuminous) particles held in suspension; 
it occurs rarely in tuberculous, endotheliomatous, and other forms of 
pleuritis. Both forms of chylothorax may be associated with similar 
disease of the peritoneum. The symptoms and physical signs are like 
those of hydro thorax, serofibrinous pleurisy, or tumor of the pleura. 
The diagnosis is usually not made until the fluid has been obtained 
by thoracentesis. It is often difficult to distinguish chylous from chyli- 
form fluid: chylous fluid contains sugar, which, however, has been 
found also in some cases of chyliform fluid; chylous fluid, as a rule, 
contains a small amount of fat (1 per cent, or less), while chyliform 



584 DISEASES OF THE MEDIASTINUM 

fluid may contain 5 to 6 per cent, or more, and its fatty and albuminous 
granules are likely to be coarser than those of chylous fluid. 



TUMORS OF THE PLEURA. 

Tumors of the pleura may be primary or secondary. The secondary 
growths usually follow primary tumors of the lungs, or mediastinum 
(extension by contiguity or lymphatic distribution), or of the kidneys 
(hypernephroma) or other organs from which metastasis may occur by 
way of the bloodvessels. The primary tumors may be benign (lipoma, 
fibroma, chondroma) or malignant — the more common endothelioma 
and the rarer sarcoma (round- or spindle-cell). They occur as flat, cir- 
cumscribed or diffuse, more or less soft growths; and cause moderate or 
considerable thickening of the pleura. Metastasis may occur to the 
lungs and other adjacent organs; and the growth may become visible 
beneath the skin. The symptoms are those of chronic pleurisy, with 
perhaps considerable local pain or distress, and progressive anemia 
and cachexia. The chest may be irregularly distended and retracted, 
and the dulness may vary in intensity here and there and be quite 
irregular in outline. The fluid removed by exploratory puncture is 
likely to be hemorrhagic, and may contain isolated tumor cells or particles 
of the growth. The prognosis is bad, the course of the disease being, 
as a rule, a few months only. The treatment is purely symptomatic — 
promotion of the comfort of the patient, relief of pain and distress by 
morphine if necessary, the removal of large collections of fluid, etc. 



DISEASES OF THE MEDIASTINUM. 

MEDIASTINITIS. 

Mediastinitis may be acute or chronic. The chronic process is usually 
part of a chronic obliterative pericarditis (mediastinopericarditis), asso- 
ciated or not with chronic obliterative pleuritis; the symptoms are 
discussed in connection with chronic adhesive pericarditis. 

Acute mediastinitis is sometimes divided, according to its location, into 
anterior and posterior, the dividing line being a plane laterally through 
the middle of the trachea. The process may be simple or suppurative 
(often two stages of the one process). It may be due to trauma; to 
inflammation of adjacent tissues (pleura, pericardium, lungs, oesophagus, 
ribs, sternum, vertebrae, connective tissue of the neck, etc.); or to infec- 
tious, especially septicopyemic, processes elsewhere in the body (hemo- 
genic infection). The lesions are those of inflammation, often asso- 
ciated with considerable oedema, which may proceed to abscess formation. 
Either the connective tissues or the lymph nodes, or both, may be 
involved, and the lesions of one or the other may predominate. The 



TUMORS OF THE MEDIASTINUM 585 

lymph nodes are especially involved in tuberculosis, syphilis, and other 
infections, such as pertussis. 

Symptoms.— The symptoms consist: (1) Fever, and perhaps initial 
chill or chilliness; (2) evidences of local inflammation, such as sub- 
sternal pain and tenderness, and perhaps oedema about the sternum, 
in the intercostal spaces, and the episternal notch; and (3) pressure 
effects, such as dyspnoea, dysphagia, etc. (more fully mentioned under 
mediastinal tumors). In the event of suppuration, irregular chills, 
fever, sweats, and leukocytosis may supervene; the pain may become 
more severe and throbbing in character, and the local effects of pressure 
more aggravated. The abscess may penetrate and ultimately perforate 
through an intercostal space, the trachea, a bronchus, the pleura, the 
oesophagus, etc., or it may burrow into the abdomen. 

Diagnosis. — The bulging sometimes caused in an intercostal space 
may be mistaken for an aneurysm, especially if it pulsates and is fluctu- 
ating; but the absence of expansile pulsation, of diastolic shock, and 
of murmurs, and the presence of the general and local evidences of 
suppuration should obviate diagnostic error. 

Treatment. — The treatment is surgical, and consists of evacuation 
and drainage. 



TUMORS OF THE MEDIASTINUM. 

Tumors of the mediastinum may be primary or secondary. The 
secondary growths (carcinomas and sarcomas) develop from extension 
of tumors of adjacent organs or represent metastases from more distant 
parts. The primary tumors comprise the exceedingly rare benign 
growths (fibroma, lipoma, chondroma, etc.), and the more common 
malignant growths, of which the most common is sarcoma; carcinoma 
is rare (despite older views to the contrary; in days gone by carcinoma 
was not well differentiated from sarcoma); rare endotheliomas have 
been reported, as well as simple and dermoid cysts. Sarcoma may 
develop from the mediastinal connective tissues or lymph nodes, or from 
the thymus; when advanced it is often difficult to determine the point 
of origin. The common types are the lymphosarcoma and the spindle- 
cell sarcoma; they form tumors of variable size and consistency, that 
more or less completely fill the mediastinum, and compress the regional 
structures and organs. 

Symptoms. — As a rule, the symptoms develop insidiously and pro- 
gress gradually. The initial symptoms in most cases consist of a hard, 
dry cough or gradually increasing dyspnoea, especially on exertion, and 
progressive failure of the general health; rarely these develop rather 
suddenly and soon become marked. There may be also a sense of 
fulness or constriction of the chest; or even actual substernal pain. 

The symptoms are due almost entirely to pressure, and they vary 
much in individual cases. Dyspnoea may result from compression of 



586 DISEASES OF THE MEDIASTINUM 

the trachea, bronchus, lung, or pneumogastric nerve. Spasm of the 
glottis, paralysis of the vocal cord, aphonia, and paroxysmal dyspnoea 
may follow irritation or paralysis of the recurrent laryngeal nerve 
(usually the left, sometimes both). The cardiac activity may be accelera- 
ted or weakened, and attacks of asthma may occur, from involvement of 
the pneumogastric nerve or compression of the heart. Cyanosis, oedema, 
and venous ectasia of the head, neck, arm, and upper chest may result 
from compression of the ascending vena cava or one of its main branches, 
and superficial anastomosis may form with tributaries of the inferior 
vena cava. Hydrothorax may result from local venous obstruction. 
Dysphagia may follow pressure on the oesophagus. Inequality of the 
pupils and unilateral sweating of the face may result from involvement 
of the sympathetic nerves. The growth occasions an irregular area 
of dulness beneath and beyond the sternum, or in the back. The 
breath sounds in a lobe or in an entire lung may be weakened from 
compression of a bronchus, or they may be bronchovesicular or bron- 
chial in character from compression of the lung. The heart becomes 
more or less displaced. The growth may erode and finally penetrate 
the sternum or project through an intercostal space, in the episternal 
notch, etc. ; and it may exhibit a pulsation (non-expansile) transmitted 
from the heart or the aorta; and it may give rise to metastatic enlarge- 
ment of the cervical lymph nodes, etc. 

Diagnosis. — The disease should be suspected in all cases of ill-under- 
stood cough and dyspnoea, especially if associated with progressive 
deterioration of health. Radiographic examination may prove of the 
greatest service, revealing a non-expansile tumor mass. The greatest 
difficulty is experienced in differentiating aneurysm of the aorta (page 
501). 

Prognosis. — Death usually ensues within six or eight months of the 
onset of symptoms. 

Treatment. — The treatment, as a rule, is symptomatic. Attempts 
to remove the growth have been made and with success in tumors of 
the thymus, and dermoid cysts. 



SECTION VIII. 
DISEASES OF THE DIGESTIVE SYSTEM. 



DISEASES OF THE MOUTH. 

STOMATITIS. 

Although different varieties of stomatitis are described, they are much 
related etiologically, and in many cases they represent different stages 
of the same anatomical process. Thus, a catarrhal stomatitis fre- 
quently proceeds to the formation of vesicles and superficial erosion 
(aphthous stomatitis), and this in turn to a well-defined ulceration 
(ulcerative stomatitis). Thrush, to which (although incorrectly) the 
term parasitic or mycotic stomatitis is sometimes restricted, is a 
catarrhal stomatitis associated with a growth of Saccharomyces 
(Oidium) albicans. Gangrenous stomatitis, however, although in 
some respects allied to the milder forms of stomatitis, is probably a 
more or less independent affection. 

Etiology .—Stomatitis may occur at any age, but is more frequent in 
poorly nourished and marantic children. Its development is much 
favored by insanitary surroundings, inattention to the hygiene of the 
mouth, mouth-breathing in patients affected with adenoids, and general 
debility from any cause. It is frequently associated with and follows 
inflammation of adjacent structures, such as the nose, pharynx, and 
especially the gastro-intestinal tract. The exciting causes are either 
infectious, toxic, mechanical, or thermic. 

Infectious stomatitis may arise as a primary or a secondary process. 
As a secondary process it is common in certain of the infectious diseases, 
such as measles, scarlatina, influenza, typhoid fever, smallpox, syphilis, 
etc.; it occurs also in the debility of old age, as well as in the adynamia of 
carcinoma, tuberculosis, profound anemia, etc. A specific bacterial 
cause has not been isolated, but it is probable that many of the more 
common bacteria which have been found in association with the lesions, 
such as pneumococci, staphylococci, streptococci, the typhoid bacillus, 
influenza bacillus, the causative factors of measles and of scarlatina, 
certain leptothrix, etc., are answerable in different cases. A special 
variety of stomatitis, thrush, to which, although incorrectly, the term 



588 DISEASES OF THE MOUTH 

parasitic or mycotic stomatis is sometimes restricted, is associated with 
infection of the mouth by Saccharomyces (Oi'dium) albicans, an organ- 
ism which, because of its polymorphism, has been described under a 
variety of names. Infection with this organism is usually preceded by 
catarrhal stomatitis, so that the disease is probably the consequence of 
mixed infection. It occurs most commonly in infants, but also, especially 
as a terminal infection, in old age, tuberculosis, diabetes, carcinoma, etc. 
Its development is facilitated by mouth breathing and the restricted 
movements of the tongue, so common in adynamic patients, which 
favor the lodgement and growth of the fungus. Infection may be trans- 
mitted directly, as by infected nipples, but it is usually acquired by 
inhalation. Further evidence of the infectious nature of some cases of 
stomatitis is found in the fact that a form of the disease, usually ulcera- 
tive in character, sometimes prevails epidemically in insanitary jails, 
tenements, asylums, barracks, camps, etc. Rarely foot-and-mouth 
disease, aphthae epizooticse, affects the buccal mucous membrane of 
human beings. Some observers have maintained that the causative 
factor of ulcerative stomatitis in human beings is allied to that causing 
foot-and-mouth disease in cattle — infection being transmitted with the 
milk; others, such as Payne, have suggested that the organism is allied 
to that of impetigo contagiosa. 

Toxic stomatitis results from the ingestion of irritant and corrosive 
poisons, such as strong acids and alkalies; from the excessive and pro- 
longed use of alcohol, tobacco, strong condiments, etc.; and sometimes 
from the medicinal or other use of mercury, arsenic, lead, the iodides, 
the bromides, etc. 

Mechanical stomatitis sometimes attends the irruption of the teeth in 
infants and children; it frequently results from the irritation caused by 
sharp foreign bodies, broken and carious teeth, the too vigorous cleansing 
of the teeth and mouth, etc. It is frequently associated with the conse- 
quences of inattention to the teeth and the resulting accumulation of 
filth, decomposing food, bacteria, incrustations, etc. — whence it is partly 
infectious in nature. 

Thermic stomatitis results from the ingestion of overheated food and 
drink, as well as from burns due to other causes. 

Pathology. — In mild cases of stomatitis the lesions are those of catarrhal 
inflammation in general — swelling, hyperemia, increase of secretion, and 
later some desquamation of the superficial epithelium. In some cases the 
inflammation may extend to the submucous tissues and give rise to thick- 
ening, oedema, and induration. In more severe cases, in addition to the 
hyperemia, there are localized areas of round-cell infiltration which lead 
to the formation of papules and later vesicles; these, losing their epi- 
thelial covering, produce circumscribed whitish patches with slightly 
elevated edges, from which within a short time well-defined erosions — 
aphthae — develop. In more severe cases the lesions proceed to ulceration 
— superficial necrosis with round-cell infiltration. In thrush the mucous 
membrane is the seat of catarrhal inflammation, upon which, in conse- 



STOMATITIS 589 

quence of the development of Saccharomyces (Oidium) albicans, small 
whitish spots resembling curdled milk and about the size of a pin's head 
develop. The fungus develops just beneath the uppermost layers of the 
surface epithelium, having first penetrated the cement substance of the 
most superficial cells, which in consequence of the growth become the seat 
of pressure atrophy. The fungus rarely penetrates to the deeper layers, 
but it has been known to reach the lymphatics and even the bloodvessels, 
and thus gain access to distant parts of the body, such as the brain, etc. 
The whitish patches, consisting of the fungus, desquamated and degen- 
erated epithelium, and debris, if removed early may leave a somewhat 
raw surface, but having existed for several days, they may be removed 
with ease and leave an almost if not quite intact mucous membrane. Of 
discrete growth at first, the fungus later may spread to all parts of the 
oral and nasal cavities, and even to the pharynx, larynx, oesophagus, and 
gastro-intestinal tract. 

Symptoms.— Clinically, the following varieties of stomatitis may be 
distinguished: (1) Catarrhal; (2) aphthous; (3) ulcerative; (4) mem- 
branous; and (5) thrush. 

Catarrhal stomatitis (simple stomatitis, erythematous stomatitis, 
pultaceous stomatitis) is characterized by local pain (burning sensations), 
heat, redness, and swelling, especially of the lips, gums, and tongue. The 
tongue exhibits indentations caused by the teeth, and its swollen papillae 
may be visible through a thick grayish or yellowish coating. The swollen 
oral mucous membrane often presents distended mucous follicles. The 
oral secretions, at first lessened, soon become much increased and are 
often irritating and acid, occasioning, especially in children, erythem- 
atous areas about the angles of the mouth. Together with decom- 
posing remnants of food, desquamated and degenerating epithelium, 
leptothrix, and other bacteria, which collect about the teeth as well 
as on the dorsum of the tongue, they give to the breath a fetid odor. 
There are unpleasant sensations of taste, thirst for cool drinks is marked, 
and suckling and mastication are painful. General symptoms are rare, 
except perhaps in young children, in whom restlessness and slight fever 
may occur. Usually the disease runs its course in from five to seven 
days. Occasionally, however, especially in alcoholic subjects and inor- 
dinate smokers, the lesions tend to become subacute or chronic. In 
these cases, the mucous membrane of the mouth becomes dark brown- 
ish red in color, somewhat thickened and opaque in scattered areas, 
and sometimes fissures develop. The subjective symptoms are usually 
slight. 

Aphthous stomatitis (follicular stomatitis, vesicular stomatitis, 
herpetic stomatitis) is characterized by the development of small super- 
ficial erosions or ulcerations (2 to 4 mm. in diameter) surrounded by a 
reddish inflammatory zone. The symptoms are those of catarrhal 
stomatitis, which is usually also present, but the local pain is perhaps more 
severe. Aphthae may come out singly or in a group; usually all appear 
within twenty-four hours. They are most numerous on the tip and edges 



590 DISEASES OF THE MOUTH 

of the tongue, and the inner aspects of the lips and cheeks; they are rare 
on the pharynx. They appear as small vesicles, which, usually within 
twenty-four hours, rupture, leaving an erosion with a grayish base and a 
slightly elevated edge. Within twenty-four or thirty-six hours this 
becomes quite sharply defined and surrounded by a narrow but distinct 
inflammatory zone. At this time they are quite painful, and although 
suggesting, they differ from, ordinary ulceration in the absence of sup- 
puration. Rarely from confluence a large ulcer is formed. The general 
symptoms consist of restlessness and slight fever or merely an aggrava- 
tion of the symptoms of the primary disorder — usually gastro-intestinal 
catarrh. The disease commonly runs its course in less than a week, 
although occasionally it is protracted by successive crops of aphthae, 
or by extension of the lesions to the fauces and pharynx. 

Ulcerative stomatitis (fetid stomatitis, putrid sore mouth, phleg- 
monous stomatitis, phagadenic stomatitis, stomacace) is a form of stom- 
atitis characterized by the development of ulceration. The cases vary 
much in severity, from the mildest to those with extensive and wide- 
spread destruction of tissue, implicating sometimes the bone. The 
mildest cases may begin as a catarrhal or herpetic stomatitis, proceed to 
ulceration, and soon result in recovery. A single small, so-called simple 
ulcer, is by no means uncommon on the mucous membrane of the lips 
and cheeks, especially in gastro-intestinal derangements, and also it is 
said in nursing women. More severe lesions sometimes occur in the 
course of certain infective diseases, such as measles, scarlatina, typhoid 
fever, pertussis, etc., especially in debilitated and emaciated children; 
they are common in scorbutus; they sometimes appear during the 
course of, and sometimes as the initial manifestation of, leukemia; and 
they not infrequently follow the administration of metallic poisons, such 
as mercury, lead, arsenic, phosphorus, as well as iodine, bromine, etc. 
Certain severe cases often appear epidemically, especially in insanitary 
jails, tenements, asylums, barracks, camps, etc. The development of the 
affection is much favored by poor and insufficient food, inattention to 
the hygiene of the mouth, the presence of carious teeth, and the winter 
season. A specific cause seems likely, but it has not yet been isolated, 
although it has been said to be allied to the cause of foot-and-mouth 
disease of cattle and to the cause of impetigo contagiosa. 

The disease begins at the margin of the gums, usually near the molar 
teeth, but especially about a carious tooth. The gums become red, 
swollen, cedematous and painful; they bleed readily, and frequently 
retract, thus exposing the teeth to the point of insertion in the jaw. The 
lesions spread to the adjacent cheek and sometimes the lip, and the 
mucous membrane becoming necrotic leads to the formation of a more 
or less extensive sphacelus and ulceration. In severe cases mucopuru- 
lent matter collects beneath the gums and gives rise to a very extensive 
sloughing, the exposed teeth loosen and may drop out, and inflammation 
and necrosis of the bone may result. In addition to the ulceration there 
is catarrhal and aphthous inflammation of the oral mucous membrane, 



STOMATITIS 591 

profuse salivation, extremely foul breath, enlargement of the regional 
lymph nodes, gastro-intestinal derangements, moderate fever (102° F.), 
etc. In some cases evidence of sepsis, including an erythematous (measly) 
rash, leukocytosis, sweats, etc., develop, and the patient emaciates 
rapidly. The majority of cases run their course in from a week to ten 
days, and terminate in recovery. Certain severe cases, however, result 
fatally. 

In mercurial stomatitis (ptyalism), in addition to the inflammation 
of the mucous membrane of the mouth, there is also inflammation of the 
salivary glands. The disease begins with a metallic taste and soreness 
of the teeth on closing them vigorously. These are soon followed by 
increased flow of saliva and tenderness and sponginess of the gums. 
The tongue becomes swollen and flabby, the breath foul, the regional 
glands enlarged, and mastication and deglutition difficult and painful. 
Should the mercury not be stopped, well-developed ulceration and necro- 
sis, with loosening and eventual falling of the teeth and necrosis of the 
bone, may ensue. 

Various other forms of ulcerative stomatitis have been described. 
Thus, Riga's disease (Riga's aphtha), common in Southern Italy and 
sometimes occurring epidemically in young (especially marantic) 
children about the time of irruption of the first teeth (lower incisors), 
consists of the development of a grayish induration, proceeding to ulcera- 
tion, situated at the frenum of the tongue. A similarly situated ulcera- 
tion sometimes occurs in pertussis from the forcible projection of the 
tongue against the lower incisor teeth during the paroxysms of coughing. 
Bednars aphtha? (aphthae of the palate) which sometimes occur in young 
marantic, especially bottle-fed babies, consist of grayish patches of super- 
ficial necrosis proceeding to ulceration of both halves of the posterior part 
of the hard palate near the alveolar processes. It is usually looked upon 
as a pressure necrosis with subsequent bacterial infection, occasioned by 
the nipple or the nurse's finger. Jacobi has described a chronic neurotic 
stomatis, in some respects akin to pemphigus vegetans, occurring in 
neurotic individuals with hereditary predispositions, and characterized 
by recurring attacks of herpetic, sometimes pemphigoid, eruption. 
Parrot has described a form of ulcerative stomatitis occurring in debili- 
tated, newly born children, and consisting of small ulcers situated sym- 
metrically on both sides of the hard palate, frequently chronic, and tend- 
ing to increase in size and involve the bone. Lemaistre has described, 
under the term la perleche, a condition consisting of painful fissures and 
elevations at the angles of the mouth, occurring epidemically, due to a 
micrococcus, and running its course in two or three weeks. 

Membranous stomatitis (croupous stomatitis) is characterized by 
the formation of a false membrane. It is usually diphtheritic in char- 
acter and due to the Klebs-Loeffler bacillus; but it sometimes results 
from the action of streptococci, staphylococci, gonococci, or Treponema 
pallidum. The local and constitutional symptoms are usually those of 
diphtheria. 



592 DISEASES OF THE MOUTH 

Thrush (parasitic stomatitis, mycotic stomatitis, soor, muguet) fs a 
form of stomatitis due to Saccharomyces (Oidium) albicans, and char- 
acterized by the development of small whitish spots which tend to 
coalesce and spread more or less extensively throughout the oral cavity. 

The disease begins usually on the dorsum of the tongue, the saccha- 
romyces, consisting of branching filaments, developing in the superficial 
layers of the mucosa, and giving rise to small whitish spots that are 
slightly elevated. As the spots become old, they tend to become dis- 
colored, yellowish, and brownish. The lesions of catarrhal and of 
aphthous stomatitis are usually associated, but the mouth is dry and the 
oral secretions usually lessened. The general symptoms are inconspicu- 
ous, and scarcely differ from those of catarrhal or of aphthous stomatitis, 
although perhaps gastro-intestinal derangements, especially diarrhoea, 
are more common. The disease, however, occurring in the course of 
other diseases, is frequently overlooked on account of the absence of 
local symptoms. Under appropriate treatment it is usually curable 
within two weeks, but it sometimes runs a protracted course. 

Diagnosis. — The diagnosis of the different varieties of stomatitis is 
usually quite obvious from an inspection of the mouth. Thrush should 
not be mistaken for milk curds nor for aphthous or ulcerative stomatitis, 
from which it is distinguished by the absence of pain and erosion or 
ulceration, and the presence of dryness of the mouth and the specific 
fungus. 

Prognosis. — The prognosis is good, at least as regards the lesions in the 
mouth. The diseases with which the stomatitis is frequently associated, 
however, often terminate fatally, the stomatitis being a local terminal 
infection. 

Treatment. — Prophylaxis is much more important than treatment as 
such. The hygiene of the mouth must be carefully attended to, especially 
in young nursing children and in the debilitated of all ages. The mouth 
should be carefully and repeatedly cleansed with bland antiseptic solu- 
tions, such as a saturated solution of boric acid in rose water, to which 
5 to 10 per cent, of glycerin may be added. Should the disease be 
developed strict cleanliness is . imperative. The causative factors in 
each case must be corrected. In the milder cases it suffices to use boric 
acid, borax, sodium bicarbonate, or potassium chlorate (2 per cent, solu- 
tions) to which 5 per cent, of tincture of myrrh may be added. Or one 
may use a mouth wash of potassium permanganate (1 per cent.) or of 
hydrogen peroxide (2 to 10 per cent.); or the following: 



1$ — Thymol 5 minims 0J3 

Oil of eucalyptus 10 minims 

Benzoic acid 1 dram 4 

Distilled water 3 ounces 100 






Miller. 



Cool drinks are usually accepted gratefully. Should aphthae develop 
they should be touched with the solid stick of silver nitrate (one applica- 
tion of which usually suffices to effect a cure), or a 5 per cent, solution of 



GANGRENE OF THE CHEEK; NOMA 593 

silver nitrate may be used. Potassium chlorate is looked upon as almost 
a specific in aphthous and ulcerative stomatitis. Locally it may be used 
in powder form, or in a 2 to 5 per cent, solution as a mouth wash; inter- 
nally, 1 to 3 grains (0.06 to 0.3 gram) carefully to a child, 10 to 20 grains 
(0.65 to 1.3 gram) to an adult, may be given three times a day. The 
following formula is serviceable: 

1^ — Potassium chlorate 2 drams 8 

Tincture of iron chloride 2 drams 8 

Camphor water 6 ounces 200(0 — M. 

S. — One tablespoonful (15 c.c.) four times a day. 

In very severe cases of ulcerative stomatitis, especially in such as 
develop epidemically, the patient should be isolated and the strictest 
antiseptic precautions carried out. The ulcerated surfaces should be 
brushed with silver nitrate (2 to 5 per cent.). 

Patients who are taking mercury should use a potassium chlorate or 
potassium permangate or other antiseptic mouth wash. Upon the devel- 
opment of stomatitis the mercury must be withdrawn, the mouth wash 
continued, and a brisk purgative administered — whereupon most cases 
subside within a few days. Should ulcers develop they should be brushed 
with silver nitrate, and potassium chlorate may be given internally. 
Atropine is often useful in controlling the excessive salivation. 

In thrush, in addition to the foregoing, especially cleanliness of the 
mouth and nursing nipples, alkaline mouth washes, such as lime water 
or sodium bicarbonate, to lessen the acidity of the secretions, and the 
withdrawal of starches and sugars from the dietary, are requisite. 
Locally, boric acid, borax, hydrogen peroxide, potassium permanganate, 
potassium chlorate, or sodium sulphite, may be used, and after the thrush 
spots have been removed the exposed mucous surface may be brushed 
with silver nitrate. In all varieties of stomatitis, but especially in thrush, 
attention must be directed to the diet, which must be nourishing, and to 
the general health, which should be improved by bitter tonics, iron, 
quinine, strychnine, cod-liver oil, etc. 



GANGRENE OF THE CHEEK; NOMA. 

(Gangrenous Stomatitis; Cancrum Oris.) 

Noma is a rapidly spreading gangrene of the cheek, usually unilateral 
and frequently terminating fatally. 

Etiology. — The disease occurs between the second and seventh years 
(although it may occur later), and in girls rather than boys, more espe- 
cially in those debilitated by certain specific infective diseases, particularly 
measles (more than one-half the cases), pertussis, typhoid fever, scar- 
latina, etc. The disease is doubtless due to infection. Recently etio- 
logical significance has been attributed to a streptothrix described by 
Perthes and Seiffert. 
38 



594 DISEASES OF THE TONGUE 

Symptoms. — The disease usually begins insidiously, commonly during 
convalescence from measles or other infective diseases, and manifests 
itself as a discolored area which soon becomes necrotic, ulcerated, and 
malodorous, and about which there speedily develop, from within 
outward, a brawny induration and often widespread oedema, involving 
the side of the face and the neck. In mild cases the ulcer remains inter- 
nal; but usually, sometimes within forty-eight or seventy-two hours, 
perforation, preceded by marked external discoloration, occurs. Some- 
times the gangrene extends to the lips, chin, even the eyes and ears, and 
may involve the bone. The adjacent bloodvessels being thrombosed, 
hemorrhage is rare, but the gangrenous area is surrounded by an in- 
flammatory zone. The regional lymph nodes are moderately enlarged, 
but local pain is not marked. The general symptoms are usually severe : 
high fever (104° F. or more), rapid pulse, extreme prostration, low mut- 
tering delirium, etc. Diarrhoea is common, and may be associated with 
colitis. Death usually ensues at the end of about a week, from toxemia 
or aspiration bronchopneumonia. 

Diagnosis. — The diagnosis is usually unmistakable. Some confusion 
with malignant pustule (anthrax) may arise, but the previous history 
of the case is different; malignant pustule is more common in adults, 
begins on the outside of the cheek, and the anthrax bacillus may be 
detected in the local lesions and in the blood. Diphtheria may be 
readily differentiated by isolating the bacillus. Ulcerative stomatitis 
can scarcely be confused with gangrene, except perhaps in the earliest 
stages. 

Prognosis. — The prognosis is bad, the mortality rate being 70 to 90 per 
cent. ; a few patients recover with extensive cicatrization and deformity. 

Treatment. — The treatment is usually unavailing. The disease is often 
far advanced before discovered. The gangrenous area must be removed 
preferably with the actual cautery, or with fuming nitric acid or the 
knife. The best results are likely to be achieved by the use of the 
actual cautery before gangrene has supervened. Subsequently strict 
antisepsis must be maintained, and the patient supported by concen- 
trated nutritious food and stimulants. I have seen diphtheria antitoxin 
do temporary good in one case occurring in typhoid fever, from which 
the diphtheria bacillus was isolated. 



DISEASES OF THE TONGUE. 

Glossitis. — Glossitis, or inflammation of the parenchyma of the tongue, 
is a rare affection, although inflammation of the lingual mucous mem- 
brane is commonly a part of stomatitis. 

Acute or parenchymatous glossitis results usually from injuries, or 
infections, or intoxications, such as mercury, the bites of insects, etc. 
The lesions, which may be unilateral, especially in the beginning, are 
those common to inflammation in general; usually they subside, but 



BLACK TONGUE 595 

they may go on to abscess formation. The symptoms consist of pain 
and extreme swelling of the tongue, which may even project beyond the 
teeth. All movements such as occur in speaking, chewing, swallowing, 
even breathing, are extremely painful, and hence restricted, at times 
almost impossible. Sloughing sometimes occurs. There may be 
moderate fever. The treatment consists in the local use of antiseptics, 
ice, cocaine, etc., general depurative measures, and surgical procedures, 
such as scarification or incision, should swelling be extreme or suppura- 
tion result. 

Chronic glossitis, usually associated with chronic stomatitis, some- 
times results from repeated acute attacks, but especially from continued 
irritation caused by carious and broken teeth, alcohol, tobacco, irritating 
food, etc. The tongue is swollen, reddened, hypersensitive, furrowed 
or fissured, and unnaturally smooth in circumscribed areas, due to 
atrophy of the papillae. A condition in which the fissures and furrows 
are unduly marked, and the tongue irregular and ragged in appearance 
and painful (on account of superficial ulcerations), is spoken of as glossitis 
desiccans. The treatment consists of the avoidance of all irritating food 
and drink, the use of antiseptic mouth washes, brushing with silver 
nitrate (5 per cent.), and tonics. 

Eczema. — Eczema of the tongue (geographical tongue, ringworm 
of the tongue, psoriasis of the tongue, tylosis of the tongue, wandering 
rash of the tongue) is a rare affection, of unknown and doubtless varying 
etiology, characterized by superficial hyperplasia and desquamation 
of the lingual epithelium. The lesions tend to heal in the centre and 
spread at the margins, giving rise to irregular circinate, map-like patches. 
The disease is chronic, and occasions only mild local symptoms, such as 
itching. The treatment consists in the use of tonics and antiseptic 
mouth washes, the local application of silver nitrate, tannic acid, alum, 
or potassium chlorate. 

Leukoplakia. — Leukoplakia of the tongue (leukoplakia oris et buccalis, 
leukoma, ichthyosis of the tongue, keratosis, smoker's tongue) is a rather 
rare disease of unknown etiology, encountered usually in inordinate 
smokers, and characterized by the development of dense, white, some- 
what elevated patches, varying in size and configuration, and situated 
usually on the tongue, rarely elsewhere on the oral mucous membrane. 
Usually smooth, the patches may become papillomatous, and even 
epithelioma may develop. The condition is chronic. The treatment, 
which is unsatisfactory, consists in the use of antiseptic mouth washes, 
and silver nitrate, chromic acid, or iodine. The use of tobacco must be 
prohibited, and to syphilitics appropriate treatment should be given. 
Should the patches become papillomatous, they should be removed. 

Black Tongue. — Black tongue (nigrities) is a rare disorder, usually 
attributed to the action of a parasite, but by some observers to benign 
tumor growth, or to intentional staining, and is characterized by the 
development of a blackish-brown discoloration of the dorsum of the 
tongue, associated with elongation of the papillae. The treatment con- 



596 DISEASES OF THE SALIVARY GLANDS 

sists of attention to the general health, and the local use of silver nitrate, 
hydrogen peroxide, salicylic acid, boric acid, etc. 

Macroglossia. — Microglossia is a condition of enlargement of the 
tongue, sometimes found in akromegaly, myxcedema, and cretinism, 
and due usually to a lymphangioma, rarely to muscular hyperplasia. 
In extreme cases operative intervention may be called for. 

Acute (Edema. — Acute oedema of the tongue, usually associated with 
oedema of the aryteno-epiglottidean fold, is a rare manifestation of urti- 
caria. Though extreme, the swelling rarely lasts more than twenty- 
four hours. Treatment must be prompt — a drastic purge, scarification, 
or leeching of the tongue, and in extreme cases, tracheotomy. 

Ranula. — Ranula is a cystic growth, situated on the under surface of 
the tongue, near the frenum, and due to dilatation of Wharton's duct, 
or to enlargement of a mucous gland. 



DISEASES OF THE SALIVARY GLANDS. 

Ptyalism. — Ptyalism (hypersecretion of the salivary glands, salivation) 
has already been mentioned as a symptom of mercurial stomatitis. 
It sometimes results also from the use of other drugs, such as gold, 
copper, iodine, tobacco, jaborandi, muscarin, etc. It occurs sometimes 
during pregnancy, rarely during menstruation; it is occasionally associ- 
ated with disease of the pancreas, variola, and rabies; and it is not in- 
frequent in certain diseases of the nervous system, such as hysteria, 
insanity, and divers diseases of the pons and medulla. The amount 
of saliva is sometimes very great (four or five liters), exceeding many times 
the normal (one to one and one-half liters). The treatment is that of 
mercurial stomatitis. 

Xerostomia. — Xerostomia (hypersecretion of the salivary glands, 
dry mouth, aptyalism), deficiency or suppression of the salivary and 
buccal secretions, is a rare condition of unknown etiology (although 
usually said to be a neurosis), occurring especially in neurotic women, 
in whom it follows sudden fright or shock. The mouth is unusually 
dry; sordes collect on the teeth and gums; the tongue may become 
fissured; and the breath is fetid. The condition is to be distinguished 
from the dry mouth of fever conditions, and that associated with the 
mouth-breathing of adenoids. Treatment is unsatisfactory, although 
oily applications locally, pilocarpin lozenges (y 1 ^- grain, 0.004 gram) 
slowly dissolved in the mouth several times daily, and galvanism locally, 
may be productive of good. 

Parotitis. — Inflammation of the parotid gland may develop, (1) as 
an acute specific infective disease — mumps (page 260); (2) as a symp- 
tomatic affection — symptomatic parotitis, parotid bubo; and (3) as a 
chronic affection. 

Acute symptomatic parotitis results from: (1) Infections, such as 
typhoid fever, typhus fever, scarlet fever, pneumococcic infection, strep- 



LUDWIG'S ANGINA 597 

tococcic infection (pyemia, erysipelas, etc.); (2) disease or injury of 
the abdominal or pelvic organs ; and (3) in association with inflammation 
of the facial nerve. In most cases the disease is infectious, the infective 
agent being carried through the blood or by way df the parotid (Sten- 
son's) duct. The inflammation is unilateral (in contradistinction to 
mumps, which is bilateral). The gland is swollen, painful, and tender, 
especially on opening the mouth, and in 50 per cent, of the cases pro- 
ceeds to suppuration. The general symptoms are moderate, as a rule 
— malaise, headache, and slight fever. The treatment consists of 
general depurative measures, and the local application of ice, leeching, 
lead water and laudanum, etc. In the event of suppuration, surgical 
measures are called for. 

Chronic parotitis rarely follows mumps, or the continued use of mer- 
cury, potassium iodide, and lead. It has been observed in chronic 
nephritis and in syphilis. Rare cases of chronic painless symmetrical 
enlargement of both parotid and lacrymal glands have been observed 
by Mikulicz (Mikulicz's disease) and others. 

Gaseous Distention.— Gaseous distention of the parotid duct and 
gland has been observed in glassblowers and musicians. 

Calculi. — Salivary calculi occasionally form in the parotid duct, and 
may give rise to distention of the duct and enlargement of the parotid 
gland. 

LUDWIG'S ANGINA. 

Ludwig's angina (angina Ludovici, cynanche gangrenosa) is a rare 
phlegmonous cellulitis of the floor of the mouth and of the neck, com- 
monly due to the streptococcus, and occurring usually as a complication 
of certain infective diseases, especially scarlet fever and diphtheria. 
It occasionally follows local trauma, and rarely occurs as an apparently 
primary affection. The symptoms, which develop and progress with 
great rapidity, consist of pain, tenderness, redness, marked swelling, 
and induration, arising usually in the neighborhood of the submaxillary 
gland on one side, and speedily involving the floor of the mouth, the 
entire neck, and even the upper part of the chest wall. The swelling of 
the tissues of the neck and an associated oedema of the glottis frequently 
give rise to an extreme, alarming, and sometimes fatal dyspnoea (asphyxi- 
ation). Extensive sloughing and gangrene are common. The general 
symptoms are those of profound sepsis (toxemia). Although the out- 
look is extremely grave, prompt surgical intervention, supportive 
measures, and antistreptococcic serum may result in cure. 



598 DISEASES OF THE FAUCES, TONSILS, AND PHARYNX 



DISEASES OF THE FAUCES, TONSILS, AND 

PHARYNX. 

ACUTE TONSILLITIS. 

(Acute Faucitis, Tonsillitis, and Pharyngitis; Sore Throat; Angina.) 

Etiology. — Acute tonsillitis, usually associated with faucitis and 
pharyngitis, may occur at any age, but is most common in adolescents, 
especially rheumatic and scrofulous subjects, and in those debilitated 
from any cause. It is especially prevalent in the spring and the early 
fall, and its development is much favored by insanitary surround- 
ings. The exciting causes are infectious, toxic, mechanical, or thermic 
irritants. Infectious angina may be primary or secondary. Most 
primary cases bear an undoubted relation to exposure or "catching 
cold." Contrary to former opinions, this is now believed to act by re- 
ducing the resistance of the tissues, thus permitting the easy operation of 
bacteria, of which the most important etiologically are the streptococcus, 
the staphylococcus, the pneumococcus, the influenza bacillus, and the 
pneumobacillus (Friedlander). An angina is also an initial manifesta- 
tion in certain specific infective diseases, such as diphtheria, scarlet 
fever, measles, etc. Secondary infectious anginas are common in other 
infective diseases, such as variola, varicella, typhoid fever, tuberculosis, 
syphilis, etc. A form of infectious angina sometimes prevails epidem- 
ically, especially in institutions, etc. Toxic anginas result from the 
inhaling of irritant vapors, such as acids and alkalies; from the excessive 
and prolonged use of alcohol, tobacco, etc. ; and from the medicinal and 
other use of mercury, the iodides, etc. Inhalation of hot vapors and 
the ingestion of too hot food and drink sometimes provokes acute 
angina. An acute angina, especially acute tonsillitis, is frequently 
the initial manifestation of a systemic infection, the infectious agent 
gaining access to the general circulation by way of the tonsils — thus 
rheumatic fever, acute endocarditis, chorea, influenza, streptococcic 
infection, tuberculosis, syphilis, etc. Recurrences are common. 

Pathology. — The lesions may involve the fauces, tonsils, and pharynx, 
singly or conjointly, and equally or unequally. In most cases all are 
more or less involved. In mild cases, the faucial and pharyngeal mucous 
membrane and submucous tissues are injected and swollen, and later 
covered with a slight amount of mucous or mucopurulent exudate 
(catarrhal faucitis, tonsillitis, or pharyngitis; sore throat). In other cases 
the tonsils present scattered yellowish-white spots — distended follicles 
filled with desquamated epithelium, leukocytes, granular debris, and 
bacteria (follicular tonsillitis). Usually the exudate can be squeezed 
from the follicles, but occasionally several adjacent follicles being dis- 
tended, the tonsil appears to be covered with a pseudomembrane, much 
simulating diphtheria. Occasionally herpes develop (herpetic tonsillitis). 



ACUTE TONSILLITIS 599 

In more severe cases the inflammation involves the substance of the 
tonsil, and usually one tonsil more than the other (parenchymatous 
tonsillitis). The affected tonsil becomes enlarged, sometimes enor- 
mously swollen, and projects far beyond the median line, rendering 
phonation, deglutition, articulation, and even respiration, extremely 
difficult. Usually the lesions soon proceed to suppuration (suppurative 
tonsillitis, quinsy), and, should surgical intervention be delayed, the 
abscess ruptures, usually through the free surface of the tonsil, rarely 
through the soft palate. At times the pus may find its way into the tissues 
of the neck or mediastinum, and may even perforate the vessels of the 
neck. Rarely more or less extensive sloughing and subsequent ulcera- 
tion of the tonsil and pseudomembranous formation occurs (ulcerative 
tonsillitis). The lesions may extend to the uvula, soft palate, and even 
the posterior pharyngeal wall, and, when occurring as a primary affection, 
they are to be distinguished from diphtheria only by the absence of the 
diphtheria bacillus. Streptococci and staphylococci are usually present 
in abundance. 

Symptoms. — Clinically one may distinguish (1) catarrhal, (2) follicular, 
and (3) suppurative or phlegmonous tonsillitis. 

Acute catarrhal tonsillitis, usually associated with faucitis and pharyn- 
gitis, is frequently sudden in onset, with chilliness, sometimes a distinct 
chill, and moderate fever. Vomiting may occur in children. An initial 
sense of dryness and irritation of the throat are soon succeeded by dis- 
tinct pain, especially upon swallowing, and a harsh, dry cough. Upon 
inspection, the tonsils, fauces, and pharynx are swollen, cedematous, 
congested, and covered with a thin layer of mucopurulent matter, which 
at the end of thirty-six or forty-eight hours is usually sufficient to give 
rise to a small amount of tenacious sputum. The general symptoms are 
mild, and the lesions subside within four or five days. 

Acute follicular (lacunar) tonsillitis is a more severe infection. The 
onset is frequently quite abrupt, with pronounced chill and high fever — 
103.5° R in adults, and frequently 105° F. in children. The faucial 
pain and tenderness and the difficulty in swallowing are usually marked, 
and there is sometimes tenderness at the angles of the jaw, on account 
of moderate swelling of the regional lymph nodes. On inspection, in 
addition to catarrhal alterations of the faucial mucous membrane, the 
tonsillar crypts are distended with a characteristic yellowish exudate, 
which, upon pressure, may be generally forced out. The constitutional 
symptoms are often quite marked, and consist of high fever, headache, 
general neuromuscular pains, depression, loss of appetite, constipation, 
etc. A trace of albumin in the urine is not uncommon. The disease 
usually runs its course in six or eight days and terminates in recovery, 
but endocarditis, pericarditis, pleuritis, erythema nodosum, etc., may 
occur as sequels. 

Acute suppurative tonsillitis (phlegmonous tonsillitis, parenchymatous 
tonsillitis, tonsillar and peritonsillar abscess, quinsy) does not differ in 
its initial local and general symptoms from those just mentioned, although 



600 DISEASES OF THE FAUCES, TONSILS, AND PHARYNX 

they are usually severe. Pain is pronounced, deglutition is extremely 
difficult, and phonation often practically impossible. On examination, 
the tonsil and adjacent tissues are found extremely swollen, congested, 
and cedematous. Not infrequently the tonsils meet in the median line; 
usually one is more inflamed than the other, and may project beyond 
the median line, displacing the markedly cedematous uvula. The glands 
at the angles of the jaw are usually swollen and tender, and there may be 
a notable fulness in the neck. The oral secretions are increased, and 
usually dribble from the mouth. Moderate leukocytosis is usually 
present. In mild cases, resolution takes place, but in perhaps one-half 
of the cases, at the end of forty-eight or seventy-two hours, fluctuation 
may be detected, and, if the tonsil be not incised, a yellowish spot of 
" pointing" soon appears and the abscess ruptures. Usually this is 
attended by great relief, and the expectoration of the pus is followed 
by speedy subsidence of the inflammatory phenomena. Rarely, however, 
the rupture occurring during sleep, for instance, may lead to suffocation; 
or the purulent matter may burrow into the tissues of the neck, and find 
its way externally through the skin, or even perforate the great blood- 
vessels of the neck; or oedema of the glottis may occur. During the 
height of the disease the general symptoms continue well marked, and 
the temperature remains high (104° F.), the pulse frequent (120 to 130 
per minute), and evidences of toxemia are found in concentration of 
the urine, slight albuminuria, prostration, perhaps delirium, etc. The 
lesions usually subside within ten days. 

Diagnosis. — The diagnosis is usually unattended by special difficulties. 
It is sometimes difficult to distinguish follicular tonsillitis from diphtheria. 
In many cases the diagnosis rests entirely upon the detection of the 
diphtheria bacillus; in some cases, however, one may distinguish follicular 
tonsillitis by the fact that the exudate is yellowish, patchy (corresponding 
to the follicles), separated by intervening areas of congested red tonsillar 
tissue, does not tend to spread beyond the tonsils, may be removed with- 
out leaving a bleeding surface, and does not tend to reform. In diph- 
theria, on the other hand, the exudate is usually grayish in color, uniform 
and widespread, tends to extend beyond the tonsils, and when removed 
tends to reform. 

Prognosis. — The prognosis is good. Most cases result in recovery, 
although recurrences are common, and hypertrophy of the tonsils 
frequently results. 

Treatment. — In all but the mildest cases the patient should go to bed 
and curtail as much as possible all movements of the throat, such as 
occur, for instance, in talking, swallowing, etc. The diet should be 
fluid. A thorough evacuation of the bowels by a generous dose of calo- 
mel (5 grains, 0.3 gram), allowed to dissolve slowly on the tongue and 
to mix with the oral secretions (whereby it may exert a local antiseptic 
action), and followed by a saline is often of value. The course of the 
disease may sometimes be shortened, in some cases apparently aborted, 
by the early administration of sodium salicylate or benzoate in large 



CHRONIC TONSILLITIS 601 

doses, 15 grains (1 gram), four or five times a day for the first twenty- 
four or thirty-six hours. In other cases, tincture of iron chloride (30 
minims, 2 c.c), quinine (2 grains, 0.13 gram), with glycerin and water, 
every four hours for thirty-six hours, seems to exert a very beneficial 
effect. Neither form of treatment, however, is of much value if begun 
when the disease is fully developed. In the case of children, full doses 
of aconite have been much praised. Locally, alkaline and mild anti- 
septic solutions may be used — such as Dobell's solution, potassium 
permanganate (2 per cent.), thymol, alum, etc., or one may use the old- 
fashioned ammoniated tincture of guaiac, in water, as.a gargle; or lozenges 
of guaiac may be dissolved slowly in the mouth. In some cases good 
results attend the local application to the tonsils of aspirin, silver 
nitrate (25 per cent.), or tincture of iron chloride, glycerin, and water. 
The comfort of the patient may also be promoted by ice locally to the 
throat and dissolved in the mouth, by the inhalation of medicated steam 
(with compound tincture of benzoin), and by the administration at night 
of a Dover's powder (10 grains, 0.6 gram). 

In extreme swelling, especially of one tonsil, such as portends suppura- 
tion, early scarification will relieve the local pain and distress. Incision 
should be practised as soon as fluctuation is apparent, even suspected. 
Cocaine (2 to 5 per cent.), menthol (2 per cent, in albolene), and hot, 
rather than cold, applications are also of service. 

During convalescence, the patient requires a nourishing diet and 
tonics, such as iron, quinine, and strychnine; or Basham's mixture and 
strychnine. Should the tonsil remain permanently enlarged (chronic 
tonsillitis), appropriate treatment must be instituted. 



CHRONIC TONSILLITIS. 

(Enlarged Tonsils; Hypertrophied Tonsils; Adenoid Vegetations; ^Chronic Naso- 
pharyngeal Obstruction; Mouth-breathing; Aprosexia.) 

Chronic tonsillitis, in which the tonsils frequently become markedly 
enlarged, is usually associated with hyperplastic alterations of the 
adenoid tissue of the pharynx (pharyngeal tonsil, Luschka's tonsil). 
The condition is of extreme importance, since it not only occasions 
nasopharyngeal obstruction and consequent mouth-breathing, but it 
exerts considerable deleterious influence on the physical and mental 
development (aprosexia) of its victims — mostly children. 

Etiology. — Hypertrophy of the tonsils and pharyngeal adenoids are 
most common between the ages of five and fifteen years. They occur in 
both sexes, but probably affect boys more than girls, especially children 
of tuberculous and syphilitic parents, and those who are poorly nourished 
and live amidst unhygienic surroundings. The affection often dates 
from an acute attack of tonsillitis, simple, diphtheritic, or scarlatinous. 

Pathology. — The lesions are those of true hypertrophy of the tonsillar 
constituents — in most cases, especially of the lymphoid tissue, in other 



602 DISEASES OF THE FAUCES, TONSILS, AND PHARYNX 

cases, of the stroma. In the first the tonsils are much enlarged (twice 
or thrice the normal size), irregular and rough on the surface, and 
exhibit distended and ruptured follicles. Although both tonsils are 
usually involved, the process may be asymmetrical. In the event of 
marked hyperplasia of the stroma, the tonsils are smaller and much 
firmer. The pharyngeal adenoids usually project from the pharyngeal 
vault, growing from the fossa of Rosenmiiller — a depression on the 
posterior pharyngeal wall between the Eustachian orifices. They 
consist of adenomatous papillomatous growths, and vary in size from 
2 to 3 mm. to 2 to 3 cm.; they are reddish in color, very vascular, 
and moderately firm. There is usually an associated chronic nasal 
catarrh; the hard palate is often unusually high, and the alveolar arch 
small. 

Symptoms. — Minor forms of chronic tonsillitis (with hypertrophy) 
may exist with no noteworthy symptoms. Sooner or later, however, 
there is interference with nasal respiration, and mouth-breathing de- 
velops. Although present during the day, this is noticed especially 
during the night, when the breathing is loud and snoring and frequently 
interrupted — whence night terrors arise. Coughing is sometimes pro- 
voked by lying down. The mouth is dry and the breath foul from 
decomposition of the exudate in the tonsillar crypts. Characteristic 
physical and mental changes soon occur. In general the child is of 
stunted growth — attributed by some authors to the embryological rela- 
tionship between the tissues of the pharynx and the pituitary body. 
The mouth is usually open, the expression becomes vacant, the bridge 
of the nose depressed, the malar prominences ill developed, the lips 
thick, the hearing defective (on account of obstruction to the Eustachian 
orifices, or extension of disease along the Eustachian tubes), the voice 
nasal, and articulation indistinct and sometimes stammering. The 
so-called pigeon-chest, or chicken-chest, frequently develops, especially 
in rachitic children. In some children with recurring asthmatic attacks 
a typical barrel-shaped or emphysematous chest may develop. Rarely a 
funnel-chest (Trickterbrust) has been observed. In advanced cases, 
marked changes in mentality occur. The child is listless, backward, 
forgetful, and seems unable to control his attention (aprosexia). He 
is sometimes morose and irritable, and complains of headache. He is 
usually weakly, anemic, and has a poor appetite, and is prone to 
recurring attacks of follicular tonsillitis, diphtheria, scarlet fever, etc. 

Diagnosis. — The affection is often disclosed by the facial, physical, 
and mental characteristics of the child. The tonsillar changes are 
quite apparent upon inspection of the throat, but the detection of the 
pharyngeal lesions, which may exist without noteworthy tonsillar changes, 
may require a rhinoscopic or digital examination. 

Prognosis. — Although the disease scarcely endangers life, it is of 
much significance in shaping the physical and mental characteristics, 
and the bad habits and general stunting that it occasions are sometimes 
not outgrown in later life. 



ULCERATION OF THE PHARYNX 603 

Treatment. — In mild cases of chronic tonsillitis the local application 
of iodine and glycerin, Lugol's solution of iodine and potassium iodide, 
tincture of iron chloride and glycerin, tannin, silver nitrate, etc., may 
prove useful. In general, however, the wise course is to remove the 
enlarged tonsils with a tonsillotome or galvanocautery, or by careful 
dissection. In all cases the pharyngeal adenoid should be immediately 
removed, with a curette or a finger, even should the child as yet not 
present the facial and mental characteristics of the disease, which will 
surely develop in the course of time. Attention to the general health, 
by suitable dress, fresh air, nutritious food, tonics, cod-liver oil, syrup 
of iron iodide, etc., is imperative. 



PHARYNGITIS. 

Acute pharyngitis, occurring independently of acute tonsillitis, is 
unusual, but is sometimes the lesion in an ordinary "sore throat." 
The symptoms and treatment are those outlined under acute tonsillitis. 

Chronic pharyngitis in children is associated with hypertrophy of 
the tonsils. In adults it is usually part of a chronic nasopharyngeal 
catarrh; it follows repeated acute attacks, and occurs especially in alco- 
holic subjects, inordinate smokers, and in those who use the voice much 
and injudiciously, such as clergymen (clergymen's sore throat), public 
speakers, singers, hucksters, etc. Several varieties have been distin- 
guished: (1) Chronic, simple, or hypertrophic nasopharyngeal catarrh; 
(2) chronic atrophic pharyngitis (pharyngitis sicca), usually associated 
with atrophy of the nasal mucous membrane; and (3) follicular or granu- 
lar pharyngitis. All three varieties are sometimes irregularly associated. 
There is usually relaxation of the faucial and pharyngeal mucous 
membrane, marked venous enlargement, and a varying amount of 
hyperplastic lymphoid tissue about the mucous follicles. The symp- 
toms are a constant sense of dryness and irritation in the throat, inter- 
fering with speaking and singing, and more or less persistent "hawking." 
In the treatment it is important to correct the cause — prohibit smoking 
and alcohol, and the too prolonged and vigorous use of the voice, etc. 
The subjective symptoms may be relieved by different mild antiseptic 
lotions or lozenges, and by the local use of silver nitrate (2 to 5 per cent.). 
Areas of glandular hypertrophy should be removed by the galvano- 
cautery. The general health should be maintained. 



ULCERATION OF THE PHARYNX. 

Ulceration of the pharynx occurs under a variety of circumstances. 
The only noteworthy symptom is pain, especially upon deglutition, but 
it varies much in different cases. Follicular ulceration is common in 
chronic catarrh — the ulcer being small and superficial. Syphilitic ulcers 



604 DISEASES OF THE FAUCES, TONSILS, AND PHARYNX 

are usually associated with mucous patches or evidences of syphilis 
elsewhere on the body; they are comparatively painless, superficial 
(unless the consequence of softening of a gumma), fairly regular in out- 
line, and respond readily to antisyphilitic treatment. Tuberculous ulcers 
are common in the later stages of tuberculosis, are exquisitely painful, 
grayish yellow in color, and irregular in outline. Rarely the infectious 
atrium in tuberculosis may be about the tonsil and take the form of an 
ulcer. In diphtheria and scarlet fever, superficial ulceration is not 
uncommon. Ulceration occurs also in lupus, in typhoid fever, variola, 
carcinoma, etc. 



Acute infectious phlegmon of the pharynx, is a term used by Senator 
to designate a rare condition in which the pharynx and the tissues of 
the neck in general become the seat of an intense inflammation that 
rapidly progresses to suppuration. The swelling and inflammatory 
oedema may be so marked as to interfere with respiration. The 
general symptoms are those of sepsis. A suppurative or phlegmonous 
pharyngitis may also follow trauma, or suppurative tonsillitis, or be 
associated with erysipelas. The treatment is surgical and supportive. 

Retropharyngeal abscess is a suppurative inflammation of the post- 
pharyngeal connective tissues. It is common in childhood, especially 
before the end of the second year, but it occurs also in adults. In children 
it frequently arises as an apparently primary infection, the infectious 
agent gaining access through any of the lymphoid tissues of that region; 
it sometimes follows diphtheria and scarlet fever. In children and in 
adults it may follow caries of the vertebrae. The symptoms,, although 
referred to the throat, are not characteristic. The diagnosis is quite 
apparent upon inspection and digital examination of the throat, although 
it may be overlooked on account of the bulging of the postpharyngeal 
wall being high up. The treatment consists of free evacuation of the 
pus, which should be done promptly, or the patient may suffocate. 

Elongation of the uvula, although frequently imaginary and occasion- 
ally congenital, sometimes results from repeated attacks of faucial in- 
flammation, and may occur in conditions of malnutrition. By irritating 
or tickling the throat on lying down, it may excite a reflex cough, or rarely 
spasm of the glottis. The treatment consists in excision, should the 
measures indicated under chronic tonsillitis not suffice. 

The lingual tonsils sometimes share in inflammatory and other dis- 
eases of the throat. Occasionally they are markedly involved, either 
alone or in association with disease of contiguous tissues, and they 
occasion pain and a feeling of fulness and discomfort at the base of the 
tongue, and a reflex cough. Occasionally they become hypertrophied 
and interfere with the actions of the epiglottis. The treatment is similar 
to that of tonsillitis. 



ULCERATION OF THE (ESOPHAGUS 605 

DISEASES OF THE (ESOPHAGUS. 

Acute Oesophagitis. — Etiology. — Oesophagitis may be due to in- 
fective, toxic, mechanical, or thermic irritants. Infective oesophagitis 
occurs in a mild or catarrhal form in many of the infective diseases, and 
at times as an extension of inflammation from the mouth and throat. 
Severer pseudomembranous forms sometimes occur in diphtheria, thrush, 
pneumonia, pyemia, etc., a pustular form may occur in smallpox. 
Toxic oesophagitis may follow the ingestion of strong acids and alkalies ; 
a chronic form is sometimes observed in those that use much alcohol or 
tobacco. Mechanical oesophagitis may result from the irritation pro- 
duced by foreign bodies. Thermic oesophagitis may follow the taking 
of overheated food or drink. 

Pathology. — The lesions vary much in different cases, and may be 
described as catarrhal, ulcerative, pseudomembranous, pustular, phleg- 
monous, and gangrenous. They exhibit no characteristics that dis- 
tinguish them from similar lesions occurring elsewhere, except that 
rarely in the pseudomembranous form casts of the oesophagus may be 
formed and perhaps expelled. 

Symptoms. — Mild oesophagitis may occasion no symptoms. Usually 
there is substernal pain, which is much aggravated by swallowing; in 
some cases with marked lesions, however, there may be little or no pain 
except on swallowing. In severe forms due to corrosive poisons, swallow- 
ing may be impossible. In some cases, especially in the event of a 
foreign body being present, attempts at swallowing occasion spasm and 
regurgitation of food. In severe cases, mucus, sometimes blood and 
pus, are ejected, and the patient emaciates. A stricture usually follows 
the oesophagitis due to corrosive poisons. 

Treatment. — The treatment is unsatisfactory. In the mild cases 
demulcent drinks and ice water may be given. Silver nitrate in solution 
and weak solutions of cocaine may prove beneficial, especially in allaying 
pain. In severe cases, feeding by the mouth should be substituted by 
enemas. 

Chronic Oesophagitis. — Chronic oesophagitis may result from an acute 
attack, or from the long-continued action of alcohol, tobacco, and other 
irritants. The mucous membrane becomes thickened and sometimes 
markedly rugous. The symptoms are more or less substernal pain, 
especially on swallowing, and perhaps regurgitation of food and mucus. 
The treatment is similar to that of acute oesophagitis. 

Ulceration. — Ulceration of the oesophagus may occur: (1) As a part 
of acute oesophagitis; (2) occasionally in cachectic states; (3) in typhoid 
fever, when it may be followed by cicatricial stenosis, and in syphilis; 
(4) in malignant disease; (5) in consequence of pressure, as by an aneu- 
rysm; and (6) as the counterpart of the round or peptic ulcer of the 
stomach. The treatment of the condition, which, however, is rarely 
recognized, is that of a causative factor, or of gastric ulcer. 



606 DISEASES OF THE (ESOPHAGUS 

Varices. — Varices of the oesophagus, usually situated at the lower 
end of the gullet, and sometimes of enormous size, may occur in cirrhosis 
of the liver and in chronic heart disease. The mucous membrane is 
the seat of chronic inflammation, and the patient may eject considerable 
mucus, but usually the condition is not recognized until a large, and 
sometimes fatal, hemorrhage occurs. 

Rupture. — Rupture of the oesophagus rarely results from the 
excessive strain of prolonged vomiting, or from weakness of the wall 
due to an ulcer. 

Dilatation. — Dilatation of the oesophagus is rare. Exceptionally it 
is primary — when it is usually congenital, but it is said to have developed 
in consequence of weakness and dilatation of the wall. In most cases 
the dilatation is secondary to, and develops above, a constriction. The 
dilatation may be fusiform or cylindrical. The chief symptoms are 
dysphagia, regurgitation of food, and loss of weight from insufficient 
nourishment. The chief aid in the diagnosis results from radiographic 
examination after the injection of bismuth or iron oxide pastes. When 
the patient can no longer get food into the stomach, he may be assisted 
with the stomach tube. Eventually rectal enemas and possibly gas- 
trostomy will be demanded. 

Diverticula. — Diverticula of the oesophagus (pharyngoceles).are of 
three kinds: (1) Congenital. (2) Pressure or pulsion diverticula, which 
are rare, arise from pressure within the oesophagus (the swallowing of large 
boluses of food), are usually situated on the posterior wall of the pharynx 
at the junction of the pharynx and oesophagus, are rarely long, and occur 
usually in adults. (3) Traction diverticula, which are not so rare, arise 
from external traction of the oesophageal wall (contraction of a cicatrix fol- 
lowing inflammation of a mediastinal lymph node), are usually situated 
on the anterior wall of the oesophagus at the bifurcation of the trachea, 
are usually quite short, and occur usually in children. Traction diver- 
ticula rarely occasion symptoms. Pressure diverticula when large may 
give rise to dysphagia, fetor of the breath (on account of decomposition 
of retained food particles, etc.), nausea, vomiting, and rarely a bulging 
on one side of the neck. The diagnosis is best made by radiographic 
examination after the injection of bismuth or iron oxide pastes. 

Spasm. — Spasm of the oesophagus (oesophagismus, spasmodic 
stricture of the oesophagus) is observed in neurotic, especially hysterical, 
subjects, and is more common in women, although it occurs in men. 
It is sometimes present during pregnancy, epilepsy, chorea, and hydro- 
phobia. The attack may develop suddenly, being provoked by violent 
emotional or other excitement. The chief complaint is of inability to 
swallow food, sometimes even liquids being rejected. An oesophageal 
bougie may be passed — sometimes immediately, sometimes after waiting 
a little for the spasm to relax and exerting slight pressure. This of 
itself may effect a lasting cure. The condition is readily recognized, as 
a rule, but in elderly subjects care must be taken not to overlook malignant 
stricture. The neurotic basis of the condition demands treatment. 



CARCINOMA OF THE (ESOPHAGUS 607 

Paralysis. — Paralysis of the oesophagus occurs in certain diseases of the 
nervous system, functional (hysteria) as well as organic (bulbar paralysis, 
general paresis, diphtheritic paralysis, etc.). The main symptom is 
dysphagia; usually also there are regurgitation of food and emaciation. 

Stenosis. — Stenosis (organic stricture) of the oesophagus may be 
congenital or acquired. Acquired stenosis may be due to: (1) Swelling 
and thickening of the oesophageal wall, such as is occasioned by inflam- 
matory (especially phlegmonous) swellings, tumors, etc.; (2) cicatriza- 
tion of ulcers produced by corrosive poisons, syphilis, typhoid fever, 
diphtheria, and the peptic or round ulcer, etc.; and (3) external pressure 
produced by an aneurysm, pericardial effusion, mediastinal tumors, 
enlarged lymph nodes, goitre, etc. Stenosis is more common in males 
than in females. It may occur anywhere throughout the oesophagus, 
but is more common in the lower third or the upper third. It may be 
moderate or extreme, and annular or vertical, and if vertical, it may 
involve a small portion or almost, if not quite, all of the oesophagus. 
The symptoms consist of gradually increasing dysphagia and regurgita- 
tion of food. At first there is perhaps mere discomfort on swallowing, 
but later sometimes inability to swallow even liquids. Regurgitation 
of food follows immediately, or after a short time, depending upon the 
situation of the stenosis. When the stenosis is near the stomach and the 
oesophagus is dilated, the delay in regurgitating the food may suggest 
that it has been vomited, but its alkalinity and the absence of gastric 
odor disprove this. Hunger and thirst are usually marked and anemia 
and emaciation soon develop. The dilatation and degree of the stenosis 
may be determined by the use of radiography or an oesophageal bougie, 
or by oesophagoscopy. It is said also that in the event of stricture, 
auscultation over the eighth or ninth thoracic vertebra will reveal a 
deglutition murmur (when the patient swallows), longer than the 
normal seven seconds. The treatment in benign cases consists in gradual 
dilatation with bougies. In some cases a tube has been inserted and 
left in situ indefinitely, the patient being fed through it. Gastrostomy 
may be resorted to in malignant cases, as well as in some that follow 
corrosive poisons. 

Carcinoma. — Carcinoma of the oesophagus occurs especially in 
men beyond the fortieth year. It is usually situated in the middle and 
lower thirds, especially at the bifurcation of the trachea. It usually 
develops from the surface epithelium (squamous-cell variety), rarely 
from the cells of the mucous glands (adenocarcinoma). It usually 
encircles the oesophagus, occasioning an annular constriction, and 
it may extend throughout a considerable portion of the oesophagus. 
Above the growth the oesophagus usually dilates and its wall hyper- 
trophies. As a rule, the carcinoma soon ulcerates, and a considerable 
portion of the necrotic tissue may be vomited, thus increasing the lumen 
again. Metastasis to the regional lymph nodes and to the nodes just 
above the clavicle, as well as extension to adjacent tissue (the mediastinum, 
lung, pleura, pericardium, vertebrae, etc.), are common, and perforation of 



608 DISEASES OF THE STOMACH 

a bronchus, or the aorta, etc., is not unknown. The symptoms consist of 
substernal pain or discomfort, gradually increasing dysphagia, regurgi- 
tation of food, and progressive emaciation with the development of the 
cancerous cachexia. The regurgitated material is frequently fetid, 
and may contain blood and pus from ulceration, and sometimes portions 
of the carcinoma itself. The development of certain pressure symp- 
toms, such as paralysis of the recurrent laryngeal nerve, oculopupillary 
phenomena, or a bronchial cough in association with oesophageal symp- 
toms, are of extreme diagnostic importance. The affection must be 
differentiated from pressure from without, as by an aneurysm, and until 
this be excluded the oesophageal bougie should not be used. The 
bougie may dislodge a portion of the growth, examination of which 
will facilitate the diagnosis. The treatment is merely supportive and 
palliative, as the disease is usually fatal within a year. Gastrostomy is 
sometimes of service. 



DISEASES OF THE STOMACH. 

Pathological Physiology. — The stomach, the most widely dilated 
portion of the digestive tract, has an average capacity in the adult of 
about 1600 c.c. (Ewald), with a normal maximum of about 2000 c.c. 
It is designed for the reception, at one time, of a considerable amount 
of food and to effect certain digestive and other changes in this food 
so as to render it suitable for further alterations in the intestine. The 
important changes, aside from the digestive, that the food undergoes 
in the stomach, comprise its conversion into a more or less fluid consist- 
ency, its being brought to a proper temperature (since the intestine 
is more sensitive to temperature variation, especially cold, than the 
stomach), and its partial sterilization by free hydrochloric acid. 

The chief functions of the stomach are secretory and motor in nature. 
The secretory activity is expressed in the gastric juice, which results 
from the influence of psychic and chemical stimuli. Mechanical stimuli, 
as a rule, induce only an increased secretion of alkaline mucus, which 
is designed primarily to protect the lining of the stomach from mechanical 
insults; the frequent repetition of these insults (bolting of large masses 
of unchewed and non-insalivated food) by irritating the stomach and 
impeding digestion, may ultimately lead to chronic gastritis. The 
psychic stimuli that promote the secretion of gastric juice comprise the 
pleasurable sensations of the sight, odor, and anticipation of food, 
often enhanced by agreeable companions and other environment — all of 
which suffice, even when the stomach is empty, to inaugurate a flow 
of gastric juice — of appetite juice as Pawlow has expressed it. The 
chemical stimuli comprise the chemical constituents of certain foods 
and condiments, such as hors d'eeuvre, meat extracts represented in 
soups, other proteins, etc. The customary arrangement of the courses 
at dinner thus finds justification in the normal physiological activities 



DISEASES OF THE STOMACH 609 

of the stomach. Starches and other carbohydrates (later courses at 
dinner) do not promote any noteworthy flow of gastric juice; they are, 
therefore, indicated in cases of excessive gastric secretion, whereas the 
aforementioned excitors of gastric juice are indicated in cases of deficient 
secretion; and it is a matter of common knowledge that an invalid with 
poor appetite can be made to eat and to digest by such environment 
as well arranged and tastefully served food. The secretion of gastric 
juice begins usually before food has entered the stomach and it continues, 
as a rule, for an hour or two thereafter, whereupon it gradually lessens. 
Variations in this, however, are common, being due to individual pecu- 
liarities, the amount and character of the food, etc., and in diseased 
states too much or too little gastric juice may be secreted — hypersecre- 
tion and hyposecretion, respectively. 

The normal gastric juice is a thin, colorless (or almost colorless) 
fluid; it has a characteristic odor, is strongly acid in reaction, and has 
a specific gravity of 1002 to 1003. Its essential constituents are hydro- 
chloric acid, pepsin (a proteolytic enzyme), rennin (lab-ferment, a milk- 
curdling enzyme), and, in small amount, lipase (a fat-splitting enzyme); 
in addition, mucin, inorganic salts, and water are found. The hydro- 
chloric acid is a product of certain so-called border or cover cells present 
in the fundic glands, which are especially numerous in the midportion 
or prepyloric region of the stomach. Normally hydrochloric acid is 
present in the gastric juice in the proportion of 0.3 per cent., although 
it may reach higher values. Expressed in terms of the amount in cubic 
centimeters of decinormal sodium hydrate solution required to neutralize 
it (the method commonly employed in clinical work), the free hydro- 
chloric acid content of the gastric juice normally varies between 20 and 
40 per hundred (which figures multiplied by 0.00365 give the actual 
hydrochloric acid percentage). The total acidity of the gastric juice, 
that is, the free hydrochloric acid, plus the combined hydrochloric acid, 
acid salts, and organic acids, normally varies between 30 and 50, with 
60 as a normal maximum. These values may be notably increased or 
decreased in disease, and hydrochloric acid may be entirely absent 
(see secretory disorders). 

Pepsin, the proteolytic enzyme of the stomach that breaks down 
proteins into albumoses and peptones, is active only in an acid medium; 
and since pepsinogen or propepsin is activated by the hydrochloric 
acid, the acidity of the gastric juice and peptic activity usually run 
parallel. At all events if the hydrochloric acid of the gastric juice is 
normal or increased, it is usually unnecessary to determine the peptic 
activity. In chronic gastritis with subacidity the peptic activity may 
be lessened; but even in this event if the mobility of the stomach remains 
effective the patient may suffer no noteworthy ill consequences. Rennin 
(lab-ferment, milk-curdling enzyme) is sometimes found deficient 
or absent in achylia gastrica, certain forms of chronic gastritis, car- 
cinoma, etc. Lipase (fat-splitting enzyme) also may be found absent 
in like circumstances. 
39 



610 DISEASES OF THE STOMACH 

As food is taken into the stomach, it is received in the fundus, the chief 
function of which is to act as a reservoir, gradually to mix the gastric 
juice with the food, and to pass the mixed food on to the pyloric portion 
of the stomach. The later portions of a large meal are received into the 
mid-portion of the mass of food already in the stomach; and since the 
movements of the fundus are not very active, contact with the gastric 
juice is only gradually effected and salivary digestion thus may continue 
for some time. The pyloric end is separated from the rest of the stomach 
by a more or less well-defined muscular band, which serves to prevent 
mixing of the food in these two portions of the organ. Food is gradually 
received into the pyloric portion through the intermediation of a pre- 
pyloric (pre-antral) or middle portion, the seat of regularly recurring 
contractions (every fifteen or twenty seconds). In the pylorus the 
muscular movements are much more active than elsewhere; here the 
food is finely comminuted, converted into a more or less fluid consist- 
ency, intimately comingled with the gastric juice, and passed on to the 
duodenum. The cause of the movements of the stomach has not been 
definitely determined; they have been ascribed to the hydrochloric acid, 
but since they occur in the entire absence of hydrochloric acid, it is not 
unlikely that they are due to the presence of the food itself; they seem 
to be myogenic in origin, but they are doubtless under the control of 
the nervous system. The intermittent opening of the pylorus and the 
discharge of the gastric contents into the duodenum also have been 
attributed to the hydrochloric acid, and the closing, to the alkalinity of 
the duodenum (Cannon). Doubtless this is a factor, but not the sole 
factor, since it occurs in the absence of hydrochloric acid and hyper- 
chlorhydria appears to be an important factor in producing pylorospasm. 
Disorders of the motility of the stomach are discussed under a separate 
heading. 

SYMPTOMATIC DISORDERS OP THE STOMACH. 

Disorders of the functions of the stomach, notably epigastric pain, 
nausea, and vomiting, are the natural consequence of definite anatomical 
lesions of the stomach of the most diverse nature, and as such they are 
usually recognized and correctly referred to a more or less obvious cause. 
In other cases, they are manifestations of disease of adjacent or other 
abdominal viscera, especially the gall-bladder, the duodenum, the 
pancreas, the vermiform appendix, and the intestine (obstruction); 
in other cases they are due to, or are part and parcel of, some general 
neurosis, such as hysteria or neurasthenia; whereas in other cases, the 
gastric symptoms seem to be due entirely to some perversion of the func- 
tional activity of the gastric nervous mechanism, and are not associated 
with discoverable anatomical lesions; in other words, the condition 
is a neurosis. 

The Appetite. — Loss or impairment of appetite (anorexia) is a symptom 
of the most diverse disorders. It is common in all diseases of the stomach, 



SYMPTOMATIC DISORDERS OF THE STOMACH 611 

although, on the contrary, even serious diseases of the stomach may exist 
with little or no impairment of the appetite. Anorexia is a character- 
istic symptom of the chronic alcoholic subject (chronic gastritis), and 
is common in many dyspeptics who, for one reason or another, have 
gradually but progressively restricted their dietary. Furthermore, the 
appetite is impaired in all fever states, in debilitated conditions (carci- 
noma, tuberculosis, prolonged suppuration), in anemic states (chlorosis, 
pernicious anemia), in nervous disorders, such as hysteria, and following 
grip, worry, excitement, etc., and it may itself be a neuroses (nervous 
anorexia). Increase of appetite (boulimia) is common in convalescents 
from acute infectious diseases, especially typhoid fever; it occurs in 
certain cases of diabetes; in pertussis (on account of the large amount 
of food often lost by vomiting); in certain cases of gastritis (after the 
anorexia passes away); and it is a manifestation of certain neurotic condi- 
tions (see sensory disorders of the stomach). 

Thirst. — Increased thirst is a common symptom of the most diverse 
disorders. It is found especially during the summer and after profuse 
sweating; in all febrile states; in xerostomia (dry mouth), arrest of 
salivary secretion; in many diseases of the stomach, especially in those 
attended by much vomiting; in diseases of the intestines characterized by 
profuse watery discharges (certain diarrhoeas, cholera, hemorrhage, etc.) ; 
and in diabetes. Persistent, increased thirst should suggest diabetes and 
lead to appropriate examinations. The contrary condition, absence of 
thirst, sometimes more apparent than real, is found in some adynamic 
febrile disorders attended by stupor, especially typhoid fever. In view 
of its importance, large amounts of water should be given to such 
patients. 

Flatulence. — The presence of an excessive amount of gases in the 
stomach may be due to several factors: (1) It may be due to the intake 
of air when eating (aerophagia). This is very common, and occurs 
especially in those who eat rapidly and bolt their food; and in nervous 
and hysterical subjects. The gases are largely those of the atmosphere, 
oxygen and nitrogen. (2) It may be due to gases taken with the food 
and drink — carbonated waters and wines, beers, etc. (3) It may 
result from fermentation of the food, which is likely to occur in the 
event of a deficiency or an absence of free hydrochloric acid, and when 
the food is retained for some time in the stomach, especially in passive 
congestion, chronic catarrhal gastritis, carcinoma and dilatation of the 
stomach, etc. In these cases one may find not only oxygen and nitro- 
gen, but also sulphuretted hydrogen, carbon dioxide, and aromatic 
products of acetic, lactic, butyric, and other forms of fermentation. 
(4) It is a common symptom in many cases of pylorospasm, often associ- 
ated with hyperchlorhydria. The condition is manifested by epigastric 
distress, pain, and distention; the pain may be quite severe and even 
colicky in nature. Relief follows belching of the gas. The treatment 
must be based upon the etiological factors; and comprises also the 
exclusion of fermentable foods, especially milk, buttermilk, potatoes, 



612 DISEASES OF THE STOMACH 

rare meat, etc., and the use of antifermentatives mentioned under the 
different types of chronic gastritis, dilatation of the stomach, etc. 

Nausea and Vomiting. — Nausea and vomiting are exceedingly 
common symptomatic complaints, and may be due to many causes. 
Usually they occur together, the nausea preceding the vomiting, but 
either may occur alone — the most distressing and persistent nausea with 
inability to vomit, and sudden vomiting without antecedent nausea. 

Etiology. — Vomiting may be due to: (1) Disease of the stomach; (2) 
disease of the abdominal viscera; (3) disease of the nervous system; (4) 
intoxications; (5) reflex disturbances; and (6) it may occur as a pure 
neuroses. 

1. The diseases of the stomach occasioning vomiting are acute and 
chronic catarrh, perigastric adhesions, ulcer, carcinoma, and dilatation. 
The vomiting of acute gastritis is often related immediately to the etio- 
logical factor, and is accompanied by epigastric pain and nausea. The 
vomited matter consists first of the gastric contents (which may reveal 
the cause of the attack), then mucus, and later bile; sometimes it is 
streaked with blood. Vomiting is a conspicuous feature of some cases 
of chronic gastric catarrh, and usually occurs in from one-half to one and 
one-half or two hours after eating. The vomited matter consists of partly 
digested food and mucus, which, being ejected, usually relieves the at- 
tendant epigastric distress and nausea. Vomiting is common in ulcer 
of the stomach, often occurs immediately on taking food, but may be 
delayed for two hours or thereabout; usually it relieves the pain which the 
taking of food may provoke, but it possesses no especial diagnostic signifi- 
cance unless accompanied by hematemesis. Vomiting is rarely missed 
in carcinoma of the stomach, but possesses no characteristic features, 
unless it is persistently of the " coffee-ground" characters. In dilatation 
of the stomach, vomiting is common; it occurs several hours after taking 
food, or at intervals of several days, is profuse, and contains stagnant 
and putrefying food. 

2. Disease of other abdominal viscera is a common cause of vomiting 
often believed to be due to disease of the stomach, especially cholecystitis 
with or without cholelithiasis, disease of the duodenum, pericholecystic, 
periduodenal, and pericolonic adhesions, acute and chronic pancreatitis, 
appendicitis, inflammatory and obstructive disorders of the intestine, 
acute and chronic peritonitis, etc. 

3. Diseases of the nervous system frequently give rise to vomiting, 
especially (a) meningitis (with or without hydrocephalus), brain tumor, 
brain abscess, and embolism, thrombosis, or hemorrhage; (6) errors of 
refraction (especially astigmatism) and of muscle balance, and Meniere's 
disease; (c) locomotor ataxia — gastric crisis; and (d) hysteria. 

4. Intoxications are a common cause of vomiting, of which the most 
important are the acute infectious diseases, such as scarlet fever, yellow 
fever, smallpox, etc.; exogenous intoxications, such as ptomaine poison- 
ing, acute alcoholism, sewer-gas poisoning, apomorphine, ipecac, ether, 
chloroform, and other drug intoxications, etc. ; and autogenic intoxica- 



SYMPTOMATIC DISORDERS OF THE STOMACH 613 

tions, such as the toxemia of pregnancy, uremia, or cholemia (diseases 
of the liver), acid intoxications that accompany diabetes and the cylic 
vomiting of children associated with ketonuria, aberrant gout, etc. 

5. Reflex vomiting is common and due to a wide variety of causes, 
such as disease of any of the thoracic or abdominal viscera, those already 
mentioned as well as renal colic, gallstone colic, intestinal colic, unpleas- 
ant odors, sights, or thoughts (in some neurotic subjects), etc. 

Vomiting without nausea is found in certain disorders of the brain, 
such as tumor or abscess and premonitory to apoplexy, in uremia and 
other autogenic poisonings, in hysteria, and as a neurosis of the stomach. 

The vomit consists at first of the contents of the stomach. In catarrh 
there is often undigested food, and there is often much mucus. The 
vomiting of watery fluid and mucus occurs also in certain nervous dis- 
orders. Bile in the vomit (bilious vomiting) occurs after repeated and 
violent vomitings, and, as a rule, has no other significance, but occasion- 
ally when appearing independently of repeated vomiting efforts it is a 
precursor of fecal vomiting. Fecal (stercoraceous) vomiting is significant 
of intestinal obstruction, but has rarely been observed in other conditions, 
such as gastrocolic fistula, and even in neurotic conditions. Purulent 
vomiting occurs in phlegmonous gastritis, or after rupture of an abscess 
into the stomach or oesophagus. Profuse vomiting occurs in gastric 
dilatation. Parasites are occasionally observed in the vomit. Blood 
is of frequent occurrence, and of varying significance. 

Hematemesis (Gastrorrhagia; Hemorrhage from the Stomach). — 
Etiology. — Hematemesis is of common occurrence and of varying 
import. The general causes, alike to those that occasion hemorrhage 
from the intestine, are such as determine hemorrhage in other parts of 
the body — purpura, scurvy, malignant (or hemorrhagic) forms of certain 
specific infections (smallpox, yellow fever, cholera, malaria, measles, 
scarlatina, diphtheria, etc.), leukemia, pernicious anemia, etc.; and it 
is rarely a manifestation of vicarious menstruation, and other neurotic 
conditions, such as hysteria, vasomotor ataxia, etc. The local causes 
are: (a) Hyperemia of the gastric vessels (or of the oesophageal plexus 
of veins), common in advanced cirrhosis of the liver, heart disease, pri- 
mary splenomegaly, etc. (6) Inflammation, erosion, and ulceration of 
the gastric mucosa, such as may be provoked by irritant poisons, etc. 
(c) Peptic or other ulceration of the stomach or duodenum, including 
tuberculous, syphilitic, and especially carcinomatous ulceration, (d) 
Changes in the vessel walls, such as occur in amyloid disease, nephritis, 
etc., may occasion hemorrhage, in some cases in consequence of the 
formation and rupture of small aneurysms, (e) Trauma, external blows 
or internal injuries, provoked by diverse kinds of foreign bodies (chicken 
bones, oyster shells, etc.). (f) Hematemesis may also be due to rupture 
of an aneurysm, or to the swallowing of blood coming from the nose, 
throat, oesophagus, or lungs (hemoptysis). 

Symptoms. — Minor hemorrhages into the stomach doubtless fre- 
quently pass unnoticed, the blood being conveyed into the intestine with 



614 DISEASES OF THE STOMACH 

the food. When large the blood is usually vomited, though some of it 
usually passes into the intestine, and, being discharged with the feces, 
may discolor the stools. As vomited the blood is usually dark in color, 
clotted, though some is fluid, is acid in reaction, and often mixed with 
food. When the hemorrhage occurs slowly, characteristic dark granular 
particles (coffee grounds) are likely to appear; when it has occurred 
suddenly and in large amount it is usually immediately ejected and 
may be quite red, though some of it is likely to be clotted. The amount 
of blood vomited varies within wide limits from a scarcely perceptible 
tinge to several quarts ; and the hemorrhage may be single or repeated, 
either in quick succession or extend over a period of days. Attending 
the hemorrhage are the usual evidences of internal bleeding, faintness, 
weakness, pallor, dimness of sight, and often collapse. Occasionally 
severe and even fatal collapse has occurred without the discharge of any 
blood by the mouth or anus. 

Diagnosis. — The many causes of hematemesis should be borne in mind, 
as well as the fact that some patients practise deception ; in case of doubt 
it is wisest to see the blood before committing one's self to the belief 
of its having occurred. Small bleedings that readily pass unnoticed 
or cannot be seen by the unaided eye, may be detected by tests for 
occult blood in the vomit or the gastric contents after a test meal, or in 
the feces. Differentiating hemoptysis may sometimes cause anxiety, but 
in hematemesis sensations of faintness and of warmth in the epigastrium 
often proceed the vomiting; the blood is usually dark in color, clotted, 
acid in reaction, and often mixed with food; the symptoms and signs 
point to disease of the abdominal viscera; and blood may be discharged 
by the bowel; whereas in hemoptysis a sensation of tickling in the throat 
often precedes the hemorrhage, faintness if it occurs follows the hemor- 
rhage, and vomiting does not occur until later; the blood is bright red, 
frothy, fluid, alkaline in reaction, and may be mixed with mucus or 
purulent expectorations; the symptoms and signs point to disease of the 
thoracic viscera; and the sputum, if there is any, may be blood-tinged 
for several days. 

Treatment. — The treatment of hematemesis depends upon the cause. 
In general it is similar to that of hemorrhage occurring in typhoid fever 
(page 59). 

Motor Disorders. — The motor disorders of the stomach may 
be irritative or depressive: on the one hand, hypermotility, peri- 
staltic unrest, spasm, and vomiting; on the other hand, atony, insuffi- 
ciency of the pylorus or of the cardia, rumination, and regurgi- 
tation. 

Hypermotility or hyperkinesis is an increased activity of the motor 
functions of the stomach whereby the chyme is discharged into the 
intestine too soon. It may occur as a primary neurosis, but is usually 
associated with hyperacidity, and with some forms of achylia gastrica. 
The condition rarely occasions any symptoms, and the diagnosis is 
to be made only by attempts to remove the gastric contents. 



SYMPTOMATIC DISORDERS OF THE STOMACH 615 

Peristaltic unrest of the stomach is a term originally applied by Kuss- 
maul to exaggerated peristaltic action on the stomach. It is especially 
common in nervous and hysterical subjects, and is often associated with 
like disorders of the intestine. The exaggerated peristaltic movements 
which often begin soon after eating, and are sometimes induced by 
emotional disturbances, give rise to loud rolling and gurgling sounds, 
which may even be heard at a distance from the patient, and occasion 
corresponding annoyance and discomfort. The movements are some- 
times visible through a thin abdominal wall. The rapid emptying of 
the stomach often leads to marked hunger, and the advent of ill-prepared 
chyme into the intestine often provokes diarrhoea. Occasionally the 
direction of the movement is the reverse of the normal — antiperistalsis, 
and the gastric contents (rarely even the intestinal contents) may be 
ejected by the mouth. The condition must be differentiated from the 
visible peristalsis of pyloric obstruction. 

Spasm of the cardia sometimes occurs in regional ulceration or carci- 
noma; and it may be provoked by the introduction of a stomach tube, 
and too hasty swallowing of food or drink, especially if too hot or too cold. 
Apparently as a pure neurosis it is sometimes observed in neuropathic 
subjects, and may be acute, recurring periodically, or chronic, developing 
after the ingestion of food. In air swallowers (aerophagia) who ordin- 
arily would discharge the air, cardiospasm is not uncommon, and if 
associated with spasm of the pylorus, sometimes leads to considerable 
painful distention of the stomach (pneumatosis), which, with the sub- 
sidence of the spasm, rapidly subsides with the occurrence of the gaseous 
eructations. 

Spasm of the pylorus is a common associate of irritative lesions of the 
pyloric end of the stomach (hyperacidity, hypersecretion, ulcer, etc.), 
and is a contributing factor in the production of pneumatosis. Whether 
it occurs as a primary disorder is still debated. The symptoms are 
pain, increased peristalsis, gastric dilatation, and vomiting. Pyloric 
spasm has been found also in children the subjects of persistent 
vomiting. 

Nervous belching or eructation is usually noisy, and, occurring par- 
oxysmally and sometimes persisting for hours, has been observed in 
neuropathic subjects (women and children). The expelled gas is usually 
the atmospheric air which had been previously swallowed or aspirated, 
and may be distinguished from the eructations of gastric disorders by the 
absence of unpleasant odor. 

Nervous vomiting is sometimes observed in hysterical subjects, being 
rather a regurgitation of the food and unattended by preliminary nausea 
and the ordinary straining efforts. Von Leyden has described a primary 
periodic vomiting characterized by sudden onset, recurrence at irregular 
intervals, and persistence for from several hours to several days, which 
he regards as a neurosis. A cyclic or periodic vomiting in children has 
also been described, and is believed to be due to acid (auto-) intoxication. 



616 DISEASES OF THE STOMACH 

Of interest in this connection is the vomiting of blood sometimes observed 
in hysterical subjects without organic disease of the stomach. 

Atony of the stomach (gastroparesis, mechanical or motor insufficiency, 
myasthenia gastrica) sometimes results from a variety of disorders which 
need not be discussed here (see dilatation of the stomach), and is 
possibly, in unusual cases, a pure neurosis. The symptoms are those 
of dilatation, which soon develops. 

Insufficiency or incontinence of the cardia may result from organic 
disease or from nervous disorder, and is recognized by involuntary 
regurgitation of food, or by rumination (merycismus) — the regurgitation 
and chewing of food as ruminants chew their cud. The last named, 
as a neurosis, is sometimes observed in neuropathic subjects — hysteria, 
idiocy, insanity, epilepsy, etc. 

Insufficiency or incontinence of the pylorus may be due to organic 
disease or nervous disorders. The condition is rare and scarcely gives 
rise to destructive symptoms, but may be recognized by finding bile and 
intestinal contents in the stomach, and by the rapid passage into the 
intestine of gas or water introduced into the stomach. 

Treatment. — The treatment of the motor disorders of the stomach is 
primarily that of any local anatomical disease with which they may 
be associated, but attention must also be paid to the common under- 
lying neuropathic condition. In many cases greatest benefit attends a 
modified rest cure, with subsequent change of climate, if possible. A 
" cure" at some one of the well-known health resorts is often of much benefit 
on account of the habits of regularity there enforced, and the attention 
directed to detail. In general the diet must be regulated to suit each 
individual patient; the bowels must be moved once daily; and rest and 
exercise in proper proportion must be enjoined. Mild hydropathic 
measures, massage, and electricity are useful adjuvants. In cases due 
to irritability of the motor apparatus sedatives conjoined with the general 
measures mentioned are of service, especially the bromides, belladonna, 
and hyoscyamus, and sometimes such simple medicinal measures as 
Hoffmann's anodyne, etc. In conditions due to diminished irritability 
of the motor apparatus, the best results attend the use of the general 
measures mentioned, but in some cases excellent results follow the use 
of strychnine, but especially tincture of nux vomica, beginning with 
15 minims (1 c.c.) and gradually increasing to 60 to 90 minims (4 
to 6 c.c.) three times a day. One must not, however, mistake mere 
atony for the weakness of overuse. Iron and arsenic are valuable in 
many cases. 

Sensory Disorders. — The sensibility of the stomach may be increased 
(hyperesthesia), diminished (anesthesia), or perverted (paresthesia). 

Hyperesthesia of the stomach, increased sensitiveness of the sensory 
nerves of the stomach, is sometimes observed in hysterical and neuras- 
thenic subjects, and is manifest by the development of epigastric distress, 
a sense of weight, burning pain, etc. — symptoms common to many gastric 
disorders, and still the gastric functions seem to be performed normally. 



SYMPTOMATIC DISORDERS OF THE STOMACH 617 

Sometimes extreme pain seems to be provoked by the smallest amount 
of food, and the patient may in consequence of a voluntary starvation 
emaciate considerably. 

Gastralgia (gastrodynia, cardialgia), an aggravated hyperesthesia, 
may be due to organic disorders of the stomach, such as ulcer or car- 
cinoma; it may be part of the gastric crisis of tabes dorsalis; and it 
may occur as a neurosis, independently of organic diseases. The last 
mentioned may occur in men or women, but is much more common in 
hysterical, neurasthenic, and anemic women, and is often associated 
with disorders of menstruation. It consists of the sudden occurrence of 
extremely severe pains in the epigastrium which radiate toward the back, 
and are likely to recur at certain intervals (in some cases at night), and 
are independent of the taking of food or other demonstrable cause. The 
attack may last from a few minutes to an hour or more, and belching, 
nausea, hiccough, etc., may be associated; but, as a rule, the functions 
of the stomach appear to be well performed: the taking of food often, 
indeed, affords temporary relief from the pain. Mental depression and 
hypochondriasis not infrequently result. Care must be taken to exclude 
gastric ulcer, gastric carcinoma, biliary colic, and the gastric crises of 
tabes. 

Anorexia, or loss of appetite, as previously mentioned, sometimes 
occurs as a pure neurosis, and is sometimes associated with an 
absence of the sense of hunger. This nervous anorexia may occur 
suddenly after psychic and emotional disturbances (shock, fright, un- 
pleasant odors, etc.), and soon passes away. A more or less chronic 
anorexia is observed in many neurotic subjects — in young girls who, fear- 
ing to become stout, from the habit of eating little engender the impossi- 
bility of eating much; and in certain elderly and rather rotund women 
in whom extreme emaciation sometimes results. 

Akoria, an absence of the sense of satiety, is occasionally observed 
in hysterical and neurasthenic subjects, and may or may not be associated 
with hyperorexia. 

Hyperorexia (boulimia, polyphagia), in addition to the conditions 
mentioned under disorders of the appetite, is sometimes seen as a pure 
neuroses in certain neuropathic subjects, hysteria, neurasthenia, Graves' 
disease, epilepsy, insanity, idiocy, etc. In consequence of the inordinate 
consumption of food, gastritis and gastric dilatation not infrequently 
result. 

Parorexia (perverted appetite, pica), a craving for unusual articles 
for food, is seen in minor grades (capriciousness) in some young children, 
in chlorosis, hysteria, pregnancy, etc. In exaggerated degree, amounting 
almost to coprophagy, it is occasionally seen in dementia, mania, idiocy, 
epilepsy, etc. 

Treatment. — The treatment of the sensory disorders is determined 
by their nature and manifestations. As in the management of motor 
disorders, attention must always be directed to the underlying basic dis- 
order. In some cases of persistent gastrodynia the full rest treatment 



618 DISEASES OF THE STOMACH 

must be carried out. Milder cases may be relieved by external applica- 
tions, such as a mustard plaster, a spice poultice, or a hot-water bag, 
cold compresses and other hydropathic applications, and remedies 
such as bismuth subnitrate or subcarbonate, Hoffmann's anodyne, 
chloroform water, aromatic spirit of ammonia, bromides, and valerian 
internally. Cocaine or carbolic acid are useful in some cases. In cases 
associated with hyperacidity (rather common) silver nitrate and 
belladonna, and other remedies mentioned under hyperchlorhydria, are 
very useful. Morphine should be avoided, but if necessary an occa- 
sional dose of codeine may be given. 

Secretory Disorders. — Although the secretion of the gastric juice is 
directly under the control of the nervous system, perversions of this secre- 
tion may not be ascribed to nervous influences alone. Variations in 
the amount and quality of the gastric juice are among the most impor- 
tant manifestations of functional and organic disease of the stomach of 
the most diverse nature; and they may occur also as a pure neurosis. 
The gastric juice may be increased or diminished in total quantity or 
in the quantity of some one or more of its constituent elements — whence 
we may distinguish the following: 

Hyperchlorhydria (hyperacidity, superacidity), the secretion of an 
abnormally abundant and abnormally acid (HO) juice during digestion, 
is a manifestation of certain organic diseases of the stomach, especially 
some cases of chronic gastritis (more particularly the cases of so-called 
dyspepsia occurring in young subjects), and almost all cases of gastric 
ulcer (in which it is quite characteristic); it is common in chlorosis; and 
it sometimes occurs as a pure neurosis in neuropathic subjects, in whom 
it may be induced by emotional disturbances, shock, etc. The ferments 
of the stomach are believed to be usually increased with hydrochloric 
acid. The hyperchlorhydria of organic disease of the stomach, notably 
ulcer, is likely to be more or less persistent, whereas that due to neurotic 
influences varies much from time to time, and is often aggravated by 
emotional disturbances. The symptoms are variable; hyperacidity may not 
produce symptoms, and symptoms commonly attributed to hyperacidity 
may occur when the hydrochloric acid is normal or even diminished. 
Other factors seem to be — hypersecretion, gastric atony (or other organic 
condition), or hypersensitiveness (hyperesthesia) of the gastric mucosa 
(often associated with general neurasthenia). Usually there is epigastric 
distress and burning (perhaps extremely severe), often associated with acid 
eructations, coming on in from one to three hours after taking food (at the 
height of digestion), and disappearing with the discharge of the chyme 
into the intestine or after vomiting (which is rare). The epigastric dis- 
tress is often associated with distention and flatulence, commonly due 
to pylorospasm. The appetite is usually good and the patient appears 
well nourished. Constipation is. the rule, but the attacks of diarrhoea 
are rather common, and are due to the irritation caused by the discharge 
into the intestine of a chyme too acid to be neutralized by the bile and 
the pancreatic juice. The motor function of the stomach is usually 



SYMPTOMATIC DISORDERS OF THE STOMACH 619 

unimpaired (empty six hours after a meal), but atony and dilatation may 
develop. Examination of the gastric contents after an Ewald test break- 
fast reveals, instead of the normal 20 to 40 hydrochloric-acid content 
and 30 to 50 total acidity, values as high as 60 to 100 or more hydro- 
chloric-acid content and 80 to 130 or more total acidity. Albumin is 
digesed rapidly; starch slowly. 

Gastrosuccorrhcea (hypersecretion; supersecretion; Reichmann's dis- 
ease; gastroxynsis, Rossbach), or an increased flow of (usually highly 
acid) gastric juice, is a perversion of the secretory function of the stomach, 
whereby the gastric juice is secreted independently of the presence of 
food in the stomach. To the hypersecretion and hyperchlorhydria a 
motor insufficiency is not infrequently added. In many cases the condi- 
tion is a pure neurosis, but it may also be caused by persistent irritation 
of the gastric mucosa — whence the term acid catarrh of the stomach, 
proposed by Jaworski and Gulzinski, may not be altogether inappropri- 
ate. The condition is usually found in neuropathic subjects, hysteria, 
neurasthenia, locomotor ataxia, etc. The increased flow may be inter- 
mittent or continuous. The intermittent form (gastroxynsis, Rossbach) 
is the rarest. The attacks occur at irregular intervals, and are charac- 
terized by severe, often colicky pain in the epigastrium, headache, and 
the vomiting of a considerable quantity of clear (or yellowish), watery, 
highly acid fluid. The attacks usually occur quite independently of 
the taking of food, last for from several hours to a day or more, and disap- 
pear rather rapidly. In the intervals the patient may be quite well, or some- 
times complain of indefinite dyspeptic complaints. Continuous gastro- 
succorrhcea is the more common disorder. The patient complains of 
epigastric distress and burning, with belching, acid eructations, and 
vomiting of highly acid, watery fluid, mixed or not with particles of 
food. In the beginning the appetite is good, but later becomes impaired; 
thirst is usually increased, and constipation is the rule, although attacks 
of diarrhoea occur. The continuation of the hypersecretion when the 
stomach contains no food often occasions increased distress and vomiting 
during the night and the early morning — which are quite characteristic. 
In consequence of the pyloric spasm (and consequent obstruction) 
induced by the highly acid gastric contents, considerable dilatation of 
the stomach results, and in long-standing cases, marked emaciation, 
even suggesting carcinoma, may ensue. The diagnosis is confirmed by 
washing and emptying the stomach in the evening, and, in the morning 
before the patient has had any food, again introducing the stomach tube 
and securing a clear fluid, acid in reaction and rapidly digesting albumin. 

Hypochlorhydria (hyposecretion ; subacidity; anacidity; hypochylia 
gastrica; achylia gastrica). — Inasmuch as the secretion of gastric juice, 
or of its hydrochloric acid content may be increased, so also may it be 
diminished. In the majority of cases there is both a diminution in the 
total amount of gastric juice as well as of the hydrochloric acid content, 
but the hydrochloric-acid content may be disproportionately diminished 
or even absent, while gastric juice is still secreted; pepsin and the curdling 



620 DISEASES OF THE STOMACH 

ferment or their zymogens are usually present. Subacidity is a feature 
of most cases of gastric catarrh, and is present from time to time in 
many cases of nervous dyspepsia. Anacidity, even an absence of 
hydrochloric acid, is found in some cases of chronic gastric catarrh, and 
in nervous dyspepsia, and it is a noteworthy feature of almost all cases 
of gastric carcinoma. Total absence of the gastric juice, achylia gastrica 
(Einhorn), was originally considered significant of complete atrophy of the 
gastric mucosa, but is now known to occur as a pure neurosis, and to be 
susceptible of cure. The symptoms vary much in different cases. Gener- 
ally they are those of chronic catarrh of the stomach with fermentation, 
but symptoms may be absent if the motor activity of the stomach remains 
normal. The condition is susceptible of accurate diagnosis only by 
analyzing the gastric contents after a test meal (absence of hydrochloric 
acid, of pepsin, and of rennin). In many cases despite the notable 
deficiency of gastric juice, the digestive functions seem to be well 
performed, a fact compatible with the demonstration recently that the 
intestine is able vicariously to perform the functions of the stomach 
when the hydrochloric-acid deficit is marked; but lienteric diarrhoea is 
not infrequent. 

Treatment. — The treatment of the secretory disorders of the stomach 
is primarily that of the underlying disease — anatomical, neurotic, or both. 
In addition, in cases of hyperacidity, regulation of the diet is of the utmost 
importance. This should be largely albuminous (meat, eggs, fish, etc.), 
and non-irritating; starches should be given in small amounts, in view 
of the marked reduction in the time of amylolytic digestion in the stomach 
caused by the prompt and excessive secretion of hydrochloric acid; fats 
are fairly well tolerated, as a rule. The drinking of moderate, and 
sometimes of considerable, amounts of water at and between meals 
is often of service — serving to dilute the highly acid gastric juice; but 
discretion must be used in advising this, bearing in mind its influence 
in gastric atony and dilatation, which may be present. Alkaline mineral 
waters are especially serviceable. Alcohol, tea, coffee, and stimulating 
condiments, and too much table salt, must be avoided. The adminis- 
tration of alkalies, such as sodium bicarbonate, magnesia, etc., at the 
height of digestion, seems to neutralize the excessive acidity, but they 
should not be given when the stomach is empty, since thus they may only 
serve to increase the acidity. In many cases the hyperchlorhydria may 
be controlled by sedatives, of which the bromides serve as a type, but 
especially silver nitrate and belladonna or hyoscyamus. Cocaine and 
codeine may prove useful in some cases. Large doses of nux vomica 
are often useful in cases associated with neurasthenia. 

In gastrosuccorrhcea, similar regulation of the diet is called for: the 
amount of water should be reduced; the meals should be reduced in 
number (as compared with hyperchlorhydria), but one should bear in 
mind that a small amount of food will sometimes almost immediately 
relieve the subjective complaints. Lavage is of the greatest service; 
one may use alkaline solutions or silver nitrate 1 to 1000. The treatment 



NERVOUS DYSPEPSIA 621 

is otherwise similar to that of hyperchlorhydria. Atropine has rendered 
excellent service in some cases. 

In subacidity and anacidity the treatment is largely that of the under- 
lying condition — gastric catarrh, carcinoma, etc. The diet should be 
carefully regulated and mixed, and should contain articles likely to 
excite secretion, condiments, etc. Meat is ill borne in many of these 
cases, and usually must be reduced to a minimum, for a time at least. 
Dilute hydrochloric acid and nux vomica (in large doses) are of 
especial value. Bitter tonics are also useful. In achylia gastrica the 
use of hydrochloric acid, nux vomica, bitter tonics, hydrotherapy, 
massage, and electricity are indicated. 



NERVOUS DYSPEPSIA. 

(Nervous Dyspepsia, Leube; Gastric Neurasthenia, Ewald.) 

Nervous dyspepsia is a syndrome made up of varying combinations 
of the gastric neuroses, a condition, however, in which the subjective 
complaints are altogether disproportionate to the anomalies of gastric 
motility and secretion. 

Etiology. — Nervous dyspepsia is ascribed to undue irritability of 
the gastric nerves, but in some cases the gastric condition is depressive 
rather than irritative. It sometimes appears as an apparently inde- 
pendent disorder; usually it is associated with other neurotic manifesta- 
tions, such as hysteria, neurasthenia, etc. ; and it may be induced in neuro- 
pathic subjects by overwork, anxiety, sexual excesses, chronic alcoholism, 
etc. It sometimes arises reflexly from disease of other organs, especially 
the eye (eye strain), and the female genitalia; it appears occasionally 
to follow infections, such as malaria; and it may develop in anemic and 
chlorotic conditions. 

Symptoms. — The symptoms are extremely variable, and this is a char- 
acteristic feature. The appetite varies considerably: sometimes it is 
normal, sometimes increased, sometimes diminished, sometimes capri- 
cious or perverted. The tongue is usually clean. Epigastric distress is 
the chief complaint. Usually it is present or at least most marked during 
digestion; it varies in intensity from slight discomfort to extreme agony; 
it may come on early or not for an hour after taking food, and it may or 
may not be dependent upon the character of the food. The pain is 
most marked when there is hyperacidity. Occasionally there is epi- 
gastric tenderness; usually cutaneous hyperesthesia. Evidences of 
motor disturbances, such as belching, pyrosis, peristaltic unrest, etc., 
are not uncommon. Nausea, rarely vomiting, and referred symptoms 
such as headache, somnolence, palpitation of the heart, etc., may be 
present. When the stomach is empty there may be complaint of weak- 
ness, headache, vertigo, tinnitus aurium, etc., and sometimes even of 
severe pain (gastralgokenosis), which fact has led Boas to distinguish 
a special form of gastric neurasthenia. The motor power of the stomach 



622 DISEASES OF THE STOMACH 

usually suffers no noteworthy deterioration, since the stomach is usually 
found empty six hours after a meal. Not infrequently there are evidences 
of neurotic disorders of the intestine — flatulence, peristaltic unrest, 
colic, constipation alternating with diarrhoea, etc. All of the symptoms 
are extremely irregular; they vary much from time to time; they develop 
slowly or suddenly, and disappear equally slowly or suddenly; and the 
attacks which may be induced by emotional or other disturbances (even 
ill humor) last varying periods. Equally variable is the condition of 
the gastric juice — subacidity, hyperacidity, and normal acidity, occurring 
from time to time, although independently of discoverable cause. The 
general health of the patient, despite the marked complaints, is often 
wonderfully preserved; but some aggravated cases are seen in lean and 
quite marantic subjects. A general hypochondriacal and neurasthenic 
habitus is" common. 

Diagnosis. — The marked variability in the complaints and in the condi- 
tion of the gastric juice, the not uncommon association of other evidences 
of neurasthenia, the long duration of the symptoms with intervals of 
good health, the dependence of attacks upon well-known emotional 
disturbances, and the absence of specific symptoms, serve to exclude 
chronic gastric catarrh, gastric ulcer, and gastric carcinoma. Frequently, 
however, serious organic disease is manifested first by evidences of 
nervous dyspepsia. 

Treatment. — The treatment is practically that of neurasthenia. Great 
difficulty is often experienced by convincing the patient that his stomach 
is capable of digesting a generous meal — which, when once accomplished, 
is soon followed by dissipation of many of the subjective complaints. 
Change of scene, of climate, and sometimes of association, are of much 
benefit in most cases. In other cases the complete or modified Weir 
Mitchell rest cure must be employed. Outdoor exercise, hydrothera- 
peutic measures, and nux vomica are very useful in other cases. I 



ACUTE CATARRHAL GASTRITIS. 

(Acute Gastritis; Acute Gastric Catarrh; Simple Gastritis; Acute Dyspepsia.) 

Acute catarrhal gastritis is an acute inflammation of the gastric 
mucous membrane, characterized by local pain and tenderness, nausea, 
vomiting, and sometimes fever. 

Etiology. — The affection occurs at all ages, and in both sexes. An 
inherited predisposition is suggested by the expression " weak stomach," 
but the "weak stomach" is frequently acquired rather than inherited. 
The gouty, the debilitated, and the subjects of chronic congestion of the 
stomach (liver cirrhosis, heart disease) are also predisposed to the dis- 
ease. The exciting cause of the disorder is summed up in the term 
dietetic indiscretions. These may consist of the eating of improper 
food, such as tainted meats, unripe fruit, etc. ; of overloading the stomach 
with too much food and drink, even of good quality; of defective masti- 



ACUTE CATARRHAL GASTRITIS 623 

cation, often due to hurried eating, "quick luncheons," imperfect teeth, 
etc.; of overindulgence in alcohol, periodical debauches, etc. Acute 
gastric catarrh may be provoked also by the use of certain drugs, such 
as the iodides, salicylates, mercury, etc., and it is common also in many 
infective diseases, and may be aggravated by injudicious dieting. 

Pathology. — The lesions are those of catarrhal inflammation in 
general — swelling and hyperemia, and increase of mucous secretion. 
Later there may be small submucous hemorrhages and superficial ero- 
sions. The cells of the mucous and peptic glands show cloudy swelling, 
and between them there is a small amount of round-cell infiltration. 
The gastric juice is deficient, and lactic and fatty acids, the consequence 
of decomposition, may be present. 

Symptoms. — In the ordinary cure of acute indigestion the symptoms 
are relatively mild, and consist of epigastric distress and tenderness, 
soon succeeded by nausea and vomiting, with some relief. The tongue 
is flabby and coated with a thick, brownish-yellow fur; there is an 
unpleasant taste in the mouth, and perhaps headache and constipation 
(biliousness). In children there may be diarrhoea, and even mild 
intestinal colic. The attack usually subsides within twenty-four hours. 
In severer cases the onset may be quite acute, sometimes with a chill 
and moderate fever. The epigastric pain and tenderness are more 
marked, and the vomiting may be repeated and persistent, and bile 
may appear in the vomited matter. There may be acid eructations 
without vomiting. The appetite is lost. Thirst is usually marked, and 
when quenched by water is often immediately followed by vomiting. 
The headache is usually well marked, the tongue coated, the breath 
fetid, and there is much prostration, and usually constipation. The 
urine is concentrated and may contain indican. The attack usually 
subsides within three or four days, but may last longer in debilitated 
subjects. 

Diagnosis. — Mild cases present no diagnostic difficulties. Some 
of the severer cases, simulating an infection at first, may be mistaken 
for typhoid fever when they occur independently of known dietetic indis- 
cretions; diagnostic difficulties are sometimes maintained by persistence 
in the use of the term "gastric fever." From typhoid fever these cases 
may be distinguished by the abrupt onset, relatively marked remissions, 
and sudden fall of the temperature, the absence of epistaxis, of enlarged 
spleen, of initial bronchitis, of roseola, and of the Gruber-Widal reaction. 
It may simulate meningitis. In children confusion with the exanthemas 
may occur, but the detecting of a rash clears the diagnosis. 

Prognosis. — The prognosis is good, but in debilitated subjects the 
disease may be unduly protracted, and as a complication of certain 
infectious diseases, heart diseases, etc., it may prove serious, even fatal. 
Recovery is usually complete, but repeated attacks may result in subacute 
or chronic gastritis. 

Treatment. — Mild cases require no special treatment, aside from 
abstention from food, and a purge of castor oil, calomel, or blue mass, 



624 DISEASES OF THE STOMACH 

followed by a saline cathartic. If there be discomfort without vomiting, 
vomiting may be promoted by warm water, or emetics like wine of ipecac 
or mustard, or lavage may be resorted too. In severe cases the patient 
should be confined to bed, food withdrawn for a day, and an initial dose of 
blue mass (5 grains, 0.3 gram), or calomel in J grain (0.008 gram) 
every fifteen minutes for eight doses, given. The epigastric distress and 
tenderness, as well as acid eructations, may be relieved by bismuth sub- 
carbonate and sodium bicarbonate, 10 grains (0.06 gram) of each, every 
two hours; or bismuth subnitrate (10 grains, 0.06 gram) and carbolic 
acid (1 minim, 0.06 c.c.) every two hours. A spice poultice to the 
epigastrium is often grateful. If the vomiting is severe and prolonged, it 
may be relieved by cocaine (J grain, 0.01 gram) in lime water every 
hour or two, if required. Morphine had best be withheld. On the second 
day peptonized milk may be commenced, in small amounts, a tablespoon- 
ful (15 c.c.) every fifteen minutes. Later, the amount may be increased 
and the intervals lengthened, and other articles of diet added. 



PHLEGMONOUS GASTRITIS. 

(Acute Suppurative Gastritis.) 

Etiology. — Phlegmonous gastritis is a rare disease, characterized by 
suppurative inflammation of the submucous and muscular coats of the 
stomach. It appears occasionally to be idiopathic, but is more common 
in association with pyemic processes, such as puerperal infection, etc. ; it 
may follow trauma, and may be associated with gastric carcinoma (Osier's 
cases). 

Pathology. — The purulent collection may be circumscribed (abscess) 
or diffuse (phlegmon). Rarely the abscess ruptures into the stomach 
cavity or the peritoneum. 

Symptoms. — The local symptoms are those of severe gastritis — epigas- 
tric pain, tenderness, nausea, vomiting; the general symptoms, those of 
sepsis — repeated chills, high fever (104° to 105° R), sweats, prostration, 
delirium, feeble pulse, leukocytosis, etc. Rarely, the pus has occasioned 
an epigastric prominence, and it may appear in the vomit. 

The diagnosis is scarcely possible, and treatment is unavailing. 



TOXIC GASTRITIS. 

Etiology. — Toxic gastritis results from the ingestion (often with 
suicidal intent) of corrosive poisons, such as strong acids and alkalies, 
as well as certain non-corrosive poisons, such as phosphorus, arsenic, 
mercury, antimony, iodine, hydrocyanic acid, alcohol, etc. 

Pathology. — In some relatively mild cases the lesions are those of a 
severe acute gastritis. The lesions due to non-corrosive poisons consist 
of fatty degeneration of the gastric tubules, with round-cell infiltration, and 



INFECTIOUS GASTRITIS 625 

foci of hemorrhage. Following the ingestion of the corrosive poisons the 
lesions vary, depending upon the concentration of the poison, from foci 
of necrosis surrounded by areas of inflammatory reaction, to the most 
severe and widespread destruction of the stomach wall, amounting in 
some cases to conversion of a large portion of the stomach into a dis- 
colored eschar, and perforation into the peritoneum. Similar lesions are 
usually found also in the mouth, pharynx, and oesophagus, and rarely 
in the duodenum. Should the patient survive, ulceration is followed 
by cicatrization and atrophy of the gastric mucosa; sometimes by hour- 
glass contraction of the stomach, stenosis of the oesophagus, etc. 

Symptoms.— In severe cases the ingestion of the poison is followed by 
extreme abdominal pain, immediate collapse, and speedy death. In 
less severe cases the symptoms consist of severe burning pain in the 
mouth, oesophagus, and stomach; swallowing is almost, if not quite, 
impossible, and vomiting and retching almost constant. The vomit 
is bloody, and sometimes contains sloughs of the stomach wall. The 
abdomen is tender and tympanitic; the urine may contain albumin and 
casts. Subcutaneous hemorrhage and delirium and convulsions may 
develop, and the patient may die in a few days from the intoxication, 
or later, from perforation of the stomach or inanition. In mild cases 
recovery may ensue. 

Diagnosis. — The diagnosis is quite apparent from the history of the 
case, and an inspection of the mouth, throat, and vomit. 

Treatment. — The treatment is that appropriate in the different poison- 
ings to which the condition may be due, especially the Use of magnesia 
with milk or egg-albumen in acid poisonings, and dilute acids in strong 
alkali poisonings, etc. Lavage may prove useful. Morphine should be 
given for the pain. In severe cases treatment is usually unavailing. 



INFECTIOUS GASTRITIS. 

The term infectious gastritis is sometimes employed to distinguish 
affections of the stomach due to certain microorganisms, and occurring 
usually in the course of certain infective diseases. In a broad sense, some 
of the cases of acute catarrhal gastritis are doubtless infective; phlegmon- 
ous gastritis is, of course, infective. Usage, however, has tended to restrict 
the term to diseases of the stomach caused by microorganisms, such as the 
diphtheria bacillus, tubercle bacillus, pneumococcus, the typhoid bacillus, 
colon bacillus, streptococcus, etc. Occasionally, especially in diphtheria, 
pneumonia, pyemia, typhus fever, smallpox, etc., the lesions go on to the 
formation of a pseudomembrane — sometimes called membranous gas- 
tritis. Rarely fungi, such as yeast fungi, Saccharomyces albicans, the 
favus fungus, etc., excite a gastritis — so-called mycotic or parasitic gas- 
tritis. The symptoms are not distinctive, and the nature of the lesions 
is not to be recognized unless, perchance, the fungus or a portion of the 
pseudomembrane is detected in the vomit. 
40 



626 DISEASES OF THE STOMACH 

CHRONIC GASTRITIS. 

(Chronic Catarrhal Gastritis; Chronic Gastric Catarrh; Chronic Dyspepsia.) 

Chronic gastritis is a chronic inflammation of the gastric mucosa 
attended by increased secretion of mucus and alterations in the gastric 
juice, and sometimes associated with impairment of the motor power, 
and different structural changes in the wall of the stomach. 

Etiology. — Chronic gastritis may follow directly on an acute attack, 
but it is more commonly due to the continuous or frequently repeated 
action of minor irritants, especially in those predisposed by constitu- 
tional or local factors. The general predisposing factors comprise anemia 
(chlorosis, pernicious anemia) and the toxic conditions and vitiation of 
the blood, inseparable from tuberculosis, gout, nephritis, diabetes, etc. 
The local predisposing factors comprise the congestive conditions 
found in cirrhosis of the liver, chronic heart disease, etc., and different 
diseases of the stomach itself, such as carcinoma, ulceration, dilatation, etc. 
The exciting cause of the condition comprises dietetic indiscretions in a 
broad sense, such as persistent hurried and irregular eating, insufficient 
mastication, too highly seasoned food, pastry, overindulgence in alcohol, 
tea, tobacco, iced drmks, soda water, etc. It is sometimes induced also 
by the long-continued use of certain drugs, such as arsenic, mercury, 
iodine, and drastic cathartics. 

Pathology. — The lesions vary considerably in different cases. In cases, 
mild and of short standing, so-called simple chronic gastritis, the mucous 
membrane is thickened, pale gray in color, somewhat congested, though 
less so than in acute gastritis, and covered by a tenacious mucus, which 
sometimes is so worked as to warrant the term mucous gastritis. Many 
dilated and enlarged veins may be visible, especially in the gastritis of 
portal obstruction, and there are frequently small areas of hemorrhage 
and pigmentation — occasionally of superficial erosion. The glands are 
usually choked with retained secretion and may enlarge to form small 
cysts. In more aggravated cases, almost, if not quite, the entire wall 
of the stomach participates in the process, and the mucous membrane 
may be thrown up into small polyp-like projections — gastritis polyposa. 
Histologically the lesions are those of interstitial inflammation with 
parenchymatous degeneration. In most cases, after the lapse of time, 
atrophic alterations, and more or less dilatation of the stomach, result — 
so-called atrophic gastritis. The mucous membrane, as well as the entire 
wall of the stomach, becomes much thinned, the gastric tubules atrophy 
and may eventually disappear and be replaced by sclerotic fibrous 
connective tissue, giving to the mucous membrane an exceedingly smooth 
appearance, which may be interrupted here and there by a small cyst. 
In rare cases the stomach becomes much diminished in size (so that its 
capacity may be only a few ounces), and its wall very much thickened 
(2 to 3 cm.) in consequence of hyperplasia of the submucosa and 
muscularis (sclerosis of the stomach). The condition may resemble a 



CHRONIC GASTRITIS 627 

diffuse infiltrating carcinoma. This and the atrophic gastritis are some- 
times spoken of as two varieties of sclerotic gastritis — the one as phthisis 
ventriculi, the other as cirrhosis (sclerosis) ventriculi. 

Symptoms. — The symptoms vary much in different cases, and in the 
same case from time to time. Usually the appetite is poor and eating 
is followed by epigastric distress and a sense, of weight and fulness 
which sometimes amounts to severe pain, and the epigastrium may be 
tender on pressure. In some cases the appetite is good; in other cases 
there is marked distress when the stomach is empty, and eating only 
augments it. Acid eructations and flatulence are frequently present 
(flatulent dyspepsia). Nausea is common, but vomiting is rather 
unusual except in aggravated cases, in alcoholic subjects (the morning 
vomiting of alcoholics), and in the event of serious gastric disease, 
such as carcinoma, ulcer, pyloric obstruction, dilatation, etc. Associ- 
ated with the gastritis there is usually more or less catarrh of the mouth 
and the intestine: the tongue is coated and its tip and margin red; there 
is an unpleasant taste in the mouth, the breath is malodorous, the 
oral and pharyngeal secretions are often increased, and constipation 
(due to deficient activity of the intestinal muscularis) is the rule, although 
diarrhoea, sometimes associated with tympanites and colic (due to the 
propulsion into the intestine of undigested and fermenting food) may 
occur. Headache, irritability, languor, and vertigo, manifestations of 
auto-intoxication, and palpitation of the heart, due also to pressure on 
the heart by the distended stomach, are common concomitants. 

In the event of vomiting, the ejected matter consists of partly digested 
and sometimes fermenting food, considerable mucus, and different 
aromatic acids (butyric, lactic, and acetic), which partly or completely 
replace the normal hydrochloric acid. The presence of considerable 
mucus suggests the term mucous gastritis. Analysis of a test breakfast 
reveals variations in the hydrochloric acid — hyperacidity (uncommon), 
subacidity (common), or anacidity (rare). Absorption from the stomach 
is slow — potassium iodide given in a capsule does not appear in the 
saliva until considerably after fifteen minutes, the average time in 
normal individuals; and the motility of the stomach is impaired — food 
may be found in the stomach as much as seven hours after the last eating. 

Atrophic or sclerotic gastritis gives rise to no characteristic symptoms. 
The symptoms are severe, as a rule, and the patient may emaciate 
rapidly. Pernicious anemia or carcinoma is frequently simulated, 
particularly as, in some cases, the small, thickened, and sclerotic stomach 
gives rise to a palpable mass in the epigastrium, and hydrochloric 
acid may be entirely absent from the gastric contents. 

Diagnosis.— The diagnosis is usually quite apparent; but it is impor- 
tant to bear in mind that the great majority of cases of supposed chronic 
dyspepsia or gastritis that are not improved by several months of well- 
directed therapy have an anatomical basis. Most of them are cases of 
gastric or duodenal ulcer, gastric carcinoma, cholecystitis with or without 
gallstone, perigastric, pericholecystic, or periduodenal adhesions, chronic 



628 DISEASES OF THE STOMACH 

pancreatitis, chronic appendicitis, cirrhosis of the liver, etc. In protracted 
cases it may be difficult to exclude carcinoma, especia ly as carcinoma 
may be preceded for years by chronic gastritis or ulcer. Rapid course, 
marked emaciation, hematemesis, severe epigastric pain, a palpable 
tumor, glandular enlargement, absence of hydrochloric acid, and the 
presence of lactic acid (after a Boas test meal), and the Oppler-Boas 
bacillus, characterize carcinoma. When a palpable tumor is present the rare 
cirrhotic stomach may be distinguished from carcinoma by the fact that 
in the one the stomach is small, whereas in carcinoma it is usually con- 
siderably dilated. 

Prognosis. — In many cases the outlook is good — with regulation 
of the diet and proper hygiene. Atrophy of the mucosa, however, since 
it cannot be repaired, may lead to grave anemia and death. 

Treatment. — The special etiological factors in each case must be cor- 
rected. Food must be taken at regular intervals; it must be eaten 
slowly and thoroughly masticated; tea, coffee, alcohol, tobacco, pastry, 
hot bread, hot cakes, fats, sweets, pork, veal, etc., must be prohibited. 
In some cases mere regulation of the diet suffices to dissipate all the 
symptoms. In other cases a strict dietetic regimen is imperative, for 
a time at least; in some cases, especially those occurring in liver cir- 
rhosis, Bright's disease, etc., a milk diet for several weeks may be tried. 
The milk should be given in stated amounts at regular intervals and 
about 2 liters in the twenty-four hours. It may be diluted with Vichy 
or lime water, or, especially in the event of nausea, sodium bicarbonate 
(5 to 10 grains 0.3 to 0.6 gram) may be added to each glassful. For a 
short time the milk may be peptonized, or buttermilk may be substituted. 
In most cases it is unnecessary to restrict the diet to milk; most patients 
can d'gest, in addition to milk, dry toast, chicken, and roasted or broiled 
red meats. Farinaceous foods, especially potatoes, and coarse vegetables 
are a fruitful source of trouble and must be interdicted, especially 
in the event of flatulence or acid eructations. As the patient improves, 
the diet may be made more liberal by the addition of eggs, broths, and rice; 
and green vegetables, such as spinach, lettuce, fruits, etc., may be 
allowed; but pastry, fried foods, coarse vegetables, strong condiments, 
and meats, such as pork and veal, must be prohibited. In general, 
fluids taken with a meal should be moderate in amount; one should 
strive for the happy medium between the senselessness of the absolutely 
dry diet and the perniciousness of the excessive amounts of fluid. Plain 
water is the best fluid. It should be partaken of freely between meals. 

The medicinal treatment should be based upon the state of the gastric 
secretion. In conditions of subacidity, dilute hydrochloric acid (15 
minims, 1 c.c), in a glassful of water, should be given with each meal. 
In many cases, however, instead of supplying the deficient hydro- 
chloric acid, we can stimulate the secretion and improve the motor power 
of the stomach with tincture of mix vomica, beginning with 15 minims 
(1 c.c.) three times a day and gradually increasing the dose to 60 minims 
(4 c.c.) or more. The bitter tonics, gentian, cinchona, quassia, calumba, 



ACUTE DILATATION OF THE STOMACH I 629 

condurango, cardamoms, etc., are extensively used, and are of value in 
improving the appetite and stimulating the secretion and motor power 
of the stomach. Digestive ferments (pepsin, pancreatic preparations, 
etc.) may be of service in supplying a deficient digestive ferment pending 
the restoration of the gastric functions, but they are less important than 
was formerly believed, the hydrochloric acid being the more important 
factor and activating the zymogens already present. In protracted cases 
silver nitrate, \ grain (0.008 gram) combined with extract of belladonna 
or hyoscyamus, \ grain (0.008 gram), three times daily, if there is much 
pain and hyperacidity, is of value. 

In many cases lavage, preferably in the morning before breakfast, 
is serviceable. In ordinary cases, plain lukewarm water, or 1 per cent, 
sodium chloride solution, may be used. In case there is much mucus, a 
5 per cent, sodium bicarbonate solution may be used, and in case of 
fermentation, a 3 per cent, boric-acid solution or a 2 per cent, salicylic- 
acid solution, may be used — depending upon the exigencies of the case. 
The lavage may be done daily or every other day, but its use should not 
be persisted in too long, lest the " stomach-tube habit" be acquired. In 
some cases the drinking of a glassful of hot water before breakfast, or 
before each meal, is a more or less satisfactory substitute for lavage. 

Excessive flatulence may be relieved by the use of bismuth, sodium 
bicarbonate, soda-mint, aromatic spirit of ammonia, chloroform water, 
magnesium oxide, carbonate, or salicylate, carbolic acid, creosote, resorcin, 
charcoal, etc. Vomiting, if marked, may be relieved by carbolic acid, 
dilute hydrocyanic acid, cerium oxalate, bismuth subnitrate or sub- 
carbonate, cocaine, lavage, etc. 



ACUTE DILATATION OF THE STOMACH. 

Acute dilatation of the stomach results usually from the rapid over- 
filling of the stomach with excessive amounts of food and drink (espe- 
cially effervescing fluids) — the development of the condition being some- 
what favored by acute and chronic catarrh of the stomach. Aggravated 
cases merit the designation acute paralytic distention of the stomach 
(Fagge), and not infrequently terminate fatally. Another and large 
series of cases follow operations and general anesthetization. Minor 
grades sometimes occur during or after certain of the infectious diseases 
— in consequence of parenchymatous degeneration of the gastric muscu- 
lature. A majority of all cases have been found to be due to obstruc- 
tions of the lower end of the duodenum by the root of the mesentery. 
The symptoms are sudden in onset, and consist of abdominal pain and 
distention, the vomiting of a large amount of bile-stained non-fecal 
fluid, collapse, and frequently death. The treatment of the aggravated 
cases consists of emptying the stomach by means of the stomach tube, 
placing the patient in the anterior prone or knee-chest position, sub- 
sequent restriction of the diet, and the use of tonics. 



630 DISEASES OF THE STOMACH 

CHRONIC DILITATION OF THE STOMACH. 

(Gastrectasis.) 

Etiology. — Chronic dilatation of the stomach — an increase in the 
capacity of the stomach associated with motor insufficiency — is especially 
common in adult life, but is not rare in rachitic children. It may be 
obstructive or non-obstructive. The causes of obstructive dilatation are : 
(1) Pyloric obstruction, which may be due to (a) intragastric factors, such 
as cicatrization of a gastric ulcer, carcinoma or other tumor, non-malig- 
nant hypertrophic stenosis of the pylorus, pyloric spasm; or (b) extra- 
gastric factors, such as compression by a tumor of the gall-bladder, liver, 
pancreas, or neighboring lymph nodes, or adhesions about the pylorus, 
and other causes (such as displaced right kidney) exerting traction and 
causing twisting or angulation of the pylorus. Similar factors operating 
on the duodenum may also cause dilatation of the stomach. Non- 
obstructive dilatation is due to atony of the muscular coat of the stomach; 
this may be (a) congenital, or (6) acquired, in consequence of re- 
peated overfilling of the stomach (beer drinkers, gluttons, the insane, 
diabetics, etc.), chronic catarrh, and other organic (especially degenera- 
tive) diseases of the stomach. It is common in tuberculosis, carcinoma, 
anemia, and other general disturbances of nutrit'on, disorders of inner- 
vation, etc. 

Pathology. — The capacity of the average normal adult stomach is 
about 1600 c.c. (Ewald), though this is subject to individual variations, 
and doubtless varies in the same individual from time to time. Some 
persons normally have an abnormally large stomach — megastria. In 
disease, however, the dilatation may be so extreme that the stomach 
occupies almost the entire abdominal cavity and attains a capacity of 
10 or more liters, especially in the obstructive forms. In obstructive 
dilatation the stomach wall is thickened in consequence of hypertrophy; 
in the non-obstructive form it is usually thinned in consequence of 
atrophy of the muscular coat. There are also the evidences of catarrhal 
or other alterations. 

Symptoms. — The symptoms vary with the cause and the degree of the 
dilatation, Minor grades, especially those due to muscular atony, may 
be symptomless. The symptoms of chronic gastric catarrh are present 
in the majority of cases, and should the dilatation be associated with 
carcinoma, the specific symptoms of carcinoma may be present. The 
dilatation itself is suggested by loss of appetite alternating with exces- 
sive appetite and thirst, acid eructations, constipation, and the vomiting 
at long intervals of large amounts of fluid and partially digested and 
stagnant food. Vomiting sometimes occurs daily, but not infrequently 
at longer intervals — three days or more; and the amount ejected 
at once may be as much as 3 liters or more. The epigastric distress, 
which often has been gradually increasing, is usually *much relieved 
by the vomiting. The vomit is malodorous and acid (due to aromatic 
acids, lactic, acetic, and butyric), and on stand ng separates into three 



CHRONIC DILATATION OF THE STOMACH 63l 

layers — the lowermost consisting of decomposing food remnants 
(food that may have been taken days, even weeks, previously); the 
middle, of a dirty, yellowish, light brownish, or grayish fluid; and 
the uppermost, of a dirty brown frothy mass. The hydrochloric acid 
content varies much, depending largely upon the associated conditions; 
it is usually diminished or absent, rarely increased. In consequence of 
the absorption of but little fluid, constipation, lessening of the amount 
of urine, and a dry skin result; in consequence of deficient nourish- 
ment the patient loses weight and strength and becomes anemic; and 
in consequence of auto-intoxication, the absorption of fermentation 
products, divers nervous disorders, such as headache, vertigo, insomnia, 
neuralgiform pains, mental depression, hypochondriasis, etc., result. 

Physical Signs. — Physical examination often reveals a prominent 
and distended abdomen (often most marked about or below the umbili- 
cus), and the outline of the enlarged stomach can often be perceived — 
the greater curvature usually below the umbilicus, often near the pubes. 
Peristaltic (occasionally antiperistaltic) waves are sometimes visible — 
and may even be palpable. Splashing sounds (clapotage) may usually 
be elicited, and sometimes even by the patient (by suddenly contracting 
the diaphragm) or other sudden motion. Percussion and auscultatory 
percussion yield definite information as to the size of the stomach. The 
most trustworthy results are obtained by inflating the empty stomach 
(by means of a stomach tube and a hand-bulb syringe or other pump). 
A stomach may be considered dilated when the vertical diameter of gas- 
tric tympany is more than 12 to 14 cm. The lower border of the stomach 
when it is dilated is, at or below the umbilicus, but one must not 
mistake a displaced for a dilated stomach. Frequently, however, the 
two conditions are associated. 

Diagnosis. — The diagnosis is usually quite obvious from the recurrent 
vomiting of large amounts of fluid and the results of inspection and of 
percussion, especially after inflation of the stomach. Gastroptosis may 
usually be excluded by the results of physical examination and the 
presence of vomiting of stagnant food. 

Piognos s. — The prognosis is favorable in most cases except those due 
to malignant obstruction of the pylorus. 

Treatment. — The most particular attention must be paid to the diet, 
which should be concentrated and readily assimilated, such as eggs, chops, 
steak, roast beef, chicken, lamb, and mutton (no coarse meats), well- 
toasted bread or Zw'eback, rice, etc., for a time, at least. Fluids should 
be reduced to a minimum, and the food should be taken in small amounts 
at rather frequent intervals, rather than larger amounts less frequently. 
The digestive processes may be aided and the comfort of the patient 
promoted by the recumbent posture for an hour or so after partaking of 
food. Gradually a more liberal diet may be permitted. In aggravated 
cases it may be necessary to put the patient to bed and give only small 
amounts of egg-albumen, peptonized milk, scraped beef, etc., for several 
days or a week. 



632 DISEASES OF THE STOMACH 

Lavage is a useful adjuvant in many cases, and is of unquestionable 
service in the beginning of the treatment. Warm water, a saline solu- 
tion, or a mild antiseptic solution (boric acid, salicylic acid) may be used. 
It serves to remove the stagnating and fermenting food, to cleanse the 
mucous membrane (removing sometimes large amounts of mucus — in 
associated catarrh), and it relieves the overloaded stomach of a great 
weight. It is wise to discontinue the lavage as soon as possible, since the 
stomach-tube habit is not without attendant evil consequences. 

Medicinal measures comprise the use of tincture of mix vomica, which 
is of the very greatest service in increasing the motor power of the 
stomach, if given in doses of 15 minims (1 c.c), three times daily, and 
gradually increased until as much as 60 minims (4 c.c.) or more is 
given three times daily. Strychnine may be used, but it appears to be 
not so useful as the tincture of nux vomica. When hydrochloric acid is 
deficient, it should be supplied for a time at least. Occasionally antifer- 
mentatives, such as carbolic acid, creosote, salicylic acid, resorcin, 
charcoal, magnesia, etc., may be called for. 

In dilatation due to benign or malignant obstruction of the pylorus, 
perigastric adhesions, and similar conditions, resort should be had to 
surgical procedures. 



ULCER OF THE STOMACH AND DUODENUM. 

(Simple, Round, Peptic, or Perforating Ulcer of the Stomach and Duodenum.) 

The term ulcer of the stomach or duodenum is somewhat inaptly 
used to designate a localized area of necrosis of the wall of the stomach 
or duodenum, resulting from lessening of vitality and consequent diges- 
tion by the gastric juice. 

Etiology. — Gastric and duodenal ulcer may occur in both sexes, and 
at all ages, even in the very young and the aged. Formerly about 60 
per cent, of the cases were believed to occur in women, but surgical 
statistics have shown that the condition is just as common if not more 
common in men. In women it occurs especially between the twentieth 
and the thirtieth year, particularly in servants, in whom it is attributed to 
anemia and their injudicious mode of eating and tasting very hot food 
(of the truth of which there is little trustworthy data). In men it is 
most common between the thirtieth and the fiftieth year, especially in 
shoemakers, tailors, and weavers, etc., in whom, with little reason, it has 
been attributed in part to pressure on the epigastrium. 

The exact cause of the necrosis is ill understood. It has been attrib- 
uted to trauma — external, internal, and that resulting from violent 
vomiting (whence, as sometimes in uremia, hemorrhagic erosion and 
ulceration may result); by Virchow to thrombosis or embolism of a 
nutrient artery, infarction, and consequent necrosis; by Pavy and 
Cohnheim to diminished alkalescence of the blood (common in anemias), 
supplemented by gastric hyperacidity and local injury to the gastric 



ULCER OF THE STOMACH AND DUODENUM 633 

mucosa; by Dallavedova to disturbances of the celiac plexus and the 
splanchnics; by Talma to disease of the pneumogastric nerve, occa- 
sioning undue muscular contraction; and by Letulle, Nauwerck, and 
Sidney Martin to bacterial infection and toxic necrosis of the gastric 
mucosa. Recently it has been suggested that in health the cells of the 
gastric mucosa produce an anti-enzyme that resists peptic digestion of the 
cells, and that this anti-enzyme may be deficient or absent in disease. 
And it has also been supposed that the system may contain a poison 
which, being eliminated, injures the gastric cells. Experimentally, ulcers 
may be produced by injecting into the stomach a gastrotoxic serum pre- 
pared by immunizing a goat, cat, or other animal to the gastric cells of 
another animal Ewald insists upon the importance of anemia and gas- 
tric hyperacidity, which are assuredly present clinically in most of the 
cases. 

The analogous duodenal ulcer is attributable to like factors. In 
addition, ulceration of the duodenum is often observed after burns of the 
skin, especially of the abdomen; it is attributable to the action of toxins 
formed in the burned skin (or, perhaps, retained on account of functional 
incapacity of the burned skin), and eliminated by the duodenal mucosa. 

Peptic ulceration of the jejunum is occasionally observed after gastro- 
enterostomy, and is attributed to the influence of acid chyme, which finds 
its way directly into the intestine. 

Pathology.— Small abrasions or hemorrhagic erosions of the gastric 
mucosa are rather common. They are perhaps not essentially different 
from the more obvious ulceration (so-called), although they usually 
heal. The gastric ulcer itself may be acute or chronic. Usually (80 
per cent, of cases) there is a single ulcer (chronic form); sometimes 
there are several, and rarely there are many ulcers (acute and chronic 
forms): I have seen more than twenty in one case. The single chronic 
ulcer is usually situated in the posterior wall toward the pylorus and 
at or near the lesser curvature (more than 80 per cent, of the cases); 
in some cases it involves and may even straddle the pylorus. The 
acute ulcer is usually small, rounded, well defined (punched out), with a 
smooth floor, and without associated induration. The chronic ulcer is 
often much larger, sometimes very large, 5, 10, or 15 cm. in diameter, 
irregular in shape, with sloping or terraced margins (funnel-like); its 
floor may be the submucous, muscular, or peritoneal coats of the 
stomach — in some cases even adjacent viscera, such as the pancreas 
or liver, to which it may have become adherent. Cicatrization usually 
results, the resulting scar being smooth if the mucous membrane only is 
involved; but the cicatrization of deeper ulcers is attended by the devel- 
opment of a puckered and stellate scar and consequent damage to the 
stomach, such as pyloric stenosis and dilatation of the stomach. The 
cicatrization of a so-called girdle ulcer may lead to hour-glass con- 
traction of the stomach; and perigastric adhesions may result in other 
deformities of the stomach, interference with its function, and persistent 
pain. Perigastric, especially posterior, adhesions, however, in many 



634 DISEASES OF THE STOMACH 

cases are a fortunate provision of nature, since they anticipate, and 
sometimes prevent, a not uncommon and frequently fatal accident — 
perforation. Perforation, when it occurs, is usually into the adhesions 
and the related organs, where it gives rise to an abscess, or into the 
lesser peritoneal cavity, where it occasions what is known as a sub- 
phrenic pyopneumothorax; or, as sometimes happens, sinuses may form 
between the stomach and the colon, duodenum, pericardium, pleura, or 
externally. Perforation of ulcers on the anterior surface of the stomach, 
where adhesions rarely form, usually gives rise to an extensive and 
rapidly fatal peritonitis. Extensive and rarely fatal hemorrhage may 
occur usually from a branch or the main artery of the lesser curvature, 
sometimes from rupture of an aneurysmal dilatation of an artery in the 
floor of the ulcer, rarely from erosion of the splenic artery, etc. More 
common bleeding is doubtless prevented by antecedent thrombosis. 
Some ulcers persist for years; recurrences are common; and carcinoma 
sometimes develops from an ulcer or its cicatrix. 

The analogous duodenal ulcer is found above the papilla. In more 
than one-half of the cases it reaches to within three-fourths inch of the 
pylorus, and in 20 per cent, of the cases it involves the margin of the 
pylorus. The appearances and the accidents, especially hemorrhage, 
perforation, and adhesions to adjacent tissues are quite analogous to 
those of gastric ulcer. 

Symptoms. — The symptoms are extremely variable. In a few cases 
(lament gastric ulcer) there are no symptoms, the ulcer being an acci- 
dental finding at the necropsy; rarely a profuse hemorrhage or a per- 
foration is the initial manifestation. In the majority of cases, however, 
definite symptoms suggesting ulcer are preceded for months or years 
by the ordinary evidences of chronic gastritis: but many of these are 
cases of already existing, that is, chronic ulcer. Ulcer is suggested by 
pain, tenderness, undue vomiting, pylorospasm, and hyperchlorhydria. 
Gaseous and acid fluid eructations, headache, faintness, and constipa- 
tion, occasionally diarrhoea, may also be present. Pain is a constant 
and characteristic symptom, although it varies much in different cases. 
It is usually severe, and may be extreme and paroxysmal (character- 
istic). It may be localized to a small spot, which is often exquisitely 
tender, near the median line in the epigastrium; it often radiates to the 
side and back, and may be associated with a spot of tenderness near the 
tenth thoracic vertebra (Boas' point). Taking food often induces or 
aggravates the pain, either immediately, or after a short time, and the 
pain persists until the stomach is relieved of food, either by vomiting or 
by its passage into the intestine ; it is sometimes very severe two or three 
hours after eating, when the acid chyme begins to pass into the intes- 
tine, thus irritating an ulcer situated at the pylorus. The pain is some- 
times relieved by firm pressure or by change of posture — permitting 
the gastric contents to gravitate away from the site of the ulcer. The 
pain is thus due to direct irritation of the ulcer by the gastric contents, 
to the peristaltic movements of the stomach, and to the hyperchlorhydria 



ULCER OF THE STOMACH AND DUODENUM 635 

(usually, though not always, present). In some cases it may also result 
from an intermittent or more or less continuous pylorospasm, which 
leading of retention of intragastric gases may cause stretching of the 
stomach or increased intragastric tension. 

Vomiting is rather common, and occurs usually at the height of the 
paroxysm of pain (from one-quarter to two hours after eating). It is not 
infrequently provoked voluntarily by the patient to relieve the intense 
pain. When perigastric adhesions have formed, vomiting may occur in 
the intervals between eating, and when dilatation (a late phenomenon) 
ensues, the characteristic vomiting of this condition results. In the ab- 
sence of dilatation, gastric digestion is usually hastened rather than 
retarded, and the vomited matter is usually small in amount, well digested, 
and has an acid taste and odor. It also, as well as a test meal, usually but 
not invariably reveals marked hyperacidity (increased hydrochloric acid) . 

Hematemesis is common — occurring clinically in about 50 per cent, 
of the cases. Some bleeding probably occurs in all cases, from irritation 
and congestion provoked by the food, distention and stretching of the 
stomach by gases (Moynihan), severe vomiting, etc., but the blood may not 
be visible macroscopically in the vomit or the stools. As a rule, the bleed- 
ing is moderate in amount, but it may be extreme (and followed by 
syncope), and it is rarely immediately fatal. The extravasation of the 
blood being, as a rule, rather slow, the blood may remain in the stomach 
for some time, and, being altered by the gastric juice, appear in the vomit 
as black, tarry masses resembling liver, or smaller particles resembling 
coffee grounds. The vomiting of a large amount of bright blood, how- 
ever, is quite significant of gastric ulcer. Altered blood often appears in 
the stools; and in a few cases, when the hemorrhage is small, it may 
appear in the stools and not in the vomit. In many cases recourse 
must be had to tests for occult blood to detect small amounts in the 
vomit or the feces. In most cases a posthemorrhagic anemia develops, 
and in some cases may become extreme. 

In some cases one may be able to palpate, through the abdominal 
wall, a mass, which may be a thickening about the ulcer, perigastric 
exudation and adhesions, enlarged regional lymph nodes, or the hyper- 
trophied pylorus resulting from long-continued spasmodic contractions. 
Loss of weight may occur in protracted cases and following large hemor- 
rhages (when it is associated with marked anemia), but many subjects 
appear fairly well nourished. 

The onset of perforation, which occurs in about 6 per ceftt. of the 
cases, is manifested by severe abdominal, usually epigastric, pain, and 
shock, and the rapid development of peritonitis, usually of the upper 
half of the abdomen, although it may become general. 

Diagnosis. — Dyspeptic symptoms, with local pain occurring par- 
oxysmally and provoked by food, circumscribed tenderness, hyper- 
chlorhydria, and hematemesis in a young woman, are unmistakable; 
but dyspeptic symptoms, without hematemesis, in a chlorotic girl or in 
a man may be difficult to interpret. The greatest diagnostic significance 



636 DISEASES OF THE STOMACH 

should be attached to the persistence of symptoms, especially of pain, 
tenderness, pylorospasm, and hyperchlorhydria, despite several months 
of well-directed therapy: such cases often believed to be merely "chronic 
indigestion," usually have an anatomical basis, which is often ulcer. 
The pain of ulcer, as contrasted with other conditions, may sometimes 
be relieved by orthoform, 10 to 30 grains (0.6 to 2 grams) at once, or 
smaller doses before meals. Some diagnostic significance has been 
attached to this. It may be difficult or impossible (and is usually unne- 
cessary since the treatment is similar) to differentiate duodenal from 
gastric ulcer, but duodenal ulcer is suggested by the male sex, later life, 
pain to the right rather than to the left of the median line, delayed after 
taking food, little or no vomiting, and blood in the stools rather than 
hematemesis. In gastralgia, as contrasted with ulcer, the pain is less 
circumscribed, occurs independently of or is relieved by food (this 
occasionally occurs in ulcer), there is less circumscribed epigastric and 
post- thoracic tenderness, there is no hematemesis, vomiting is uncom- 
mon, the general nutrition of the patient suffers little if at all, and there 
are periods of entire relief from symptoms. The pain of biliary colic 
may be distinguished by its sudden onset, usually extreme severity, short 
duration, and sudden cessation, enlargement and tenderness of the liver 
and gall-bladder, and possible jaundice, fever, and leukocytosis. The 
hematemesis of cirrhosis of the liver maybe distinguished by its marked 
preference for the male sex, certain etiological factors (especially alco- 
hol), and associated liver conditions. The hematemesis of chronic 
gastric catarrh, especially that occurring in the aged, and that attrib- 
uted to gastric erosions, is usually difficult of differentiation, but in 
erosions hematemesis is less marked, the pain is less severe and burning 
in character, subacidity rather than hyperacidity is likely to be present, 
and, as maintained by Einhorn, shreds of the gastric mucosa may be 
found in the vomit or the washings after lavage. Attempts have been 
made to determine the site of the ulcer by noting the influence of 
posture on the pain (different postures causing the food to come in 
contact with and irritate the ulcer, or to gravitate away from it); and 
a palpable induration has been deemed significant of ulcer on the 
anterior wall, and pain in the back significant of ulcer of the posterior 
wall — but these signs are untrustworthy. 

Prognosis. — Most patients recover, but the disease usually runs a 
protracted course, relapses are common, and large hemorrhages and per- 
forations are to be dreaded; cicatrization of an ulcer may cause pyloric 
obstruction and dilatation or hour-glass contracture of the stomach, 
or may be followed by carcinoma; and perigastric adhesions may be a 
source of continued pain and ill health. 

Treatment. — Absolute rest in bed for the patient for at least four 
weeks, and rest for the stomach secured by rectal feeding for at least 
seven days, are of prime importance. Rarely it may be deemed 
desirable to begin feeding by the stomach at the end of three or four 
days. The rectal enemas may consist of peptonized milk, 4 ounces 



ULCER OF THE STOMACH AND DUODENUM 637 

(120 c.c), the whites of one or two eggs, a pinch of salt, and 5 minims 
(0.3 c.c.) of deodorized tincture of opium. This may be injected high 
up in the rectum or in the sigmoid every six or eight hours, and should 
be preceded by a cleansing enema. When feeding by the mouth is 
commenced the food must be very bland, and neither too hot nor too 
cold. Milk is the best food. At first it should be peptonized or 
pancreatinized, and given in small amounts at regular intervals — in 
ordinary cases, 2 to 4 ounces, and later 4 to 6 ounces, every three hours. 
To counteract the hyperacidity, sodium bicarbonate or calcined mag- 
nesia may be added to the milk. Buttermilk is sometimes an excellent 
substitute. Soon two to four or six raw eggs daily may be added to the 
milk, and beef juice, thin gruels, arrowroot, strained broths, potato 
puree, etc., may be given. In the early days of the treatment undue 
thirst may be relieved by enteroclysis. At the end of three or four 
weeks from the time of beginning feeding by the mouth, scraped beef, 
sweetbread, tender chicken, and similar articles of diet may be allowed; 
but care and discretion must be enjoined for at least three months. 

An essential feature of the treatment is regulation of the bowels, 
which should be opened once daily — preferably by the use of saline 
cathartics. These do good not only by clearing the bowel, but also 
(and this is the philosophy of their use in large amounis) by counter- 
acting the hyperacidity, and by their depurative action relieving the 
commonly associated gastro-intestinal catarrh. 

In many cases, aside from the foregoing, no medicines are required — 
unless pain is severe. Leube speaks highly of the local use (to the epi- 
gastrium) of boric-acid ointment and hot flaxseed poultices (changed 
every fifteen minutes) during the day, and a cold-water compress during 
the night — in relieving the epigastric pain and distress. Hemorrhage 
(blood in the bowels, as well as hematemesis) is a contra-indication to the 
use of the poultices. In cases of severe pain, however, I am rather partial 
to the use for a short time of opium, which should be combined with 
silver nitrate, giving three times daily a pill of silver nitrate, J grain 
(0.015 gram), and extract of opium, i to £ grain (0.008 to 0.015 gram). 
If the pain is not severe, I substitute hyoscyamus or belladonna for the 
opium. The bromides also are useful in relieving the pain and in 
checking hyperacidity. Codeine or cocaine may be used for the same 
purpose; and these, as well as cerium oxalate, hydrocyanic acid, chloro- 
form, ether, etc., are Useful in protracted vomiting. Bismuth in large 
doses (30 to 60 grains, 2 to 4 grams, three times daily) has been highly 
recommended, but it probably exerts more beneficial influence on 
the associated catarrh than on the ulcer, and it often gives rise to the 
most annoying constipation. Olive oil in large doses has been recom- 
mended by Cohnheim. 

In the event of severe hemorrhage the patient must be confined to 
bed absolutely at rest; an ice bag may be applied lightly to the epi- 
gastrium, and morphine, £ grain (0.015 gram), should be administered 
hypodermically. Tannic acid, gallic acid, lead acetate, ergot, Monsel's 



638 DISEASES OF THE STOMACH 

solution of iron sulphate, are of doubtful utility; but 30 minims (2 c.c.) 
of adrenalin chloride (1 to 1000) may be administered with the hope 
that it may do good. Hypodermoclysis should be resorted to in large 
hemorrhages to restore the volume of fluid lost. 

The surgical treatment of gastric ulcer has to be considered in many 
cases. Operation may be said to be indicated : (1) In recurring hemor- 
rhages uncontrolled by medicinal measures; (2) in intractable cases with 
severe pain, persistent vomiting, hematemesis, and resulting emaciation; 
(3) when perforation has occurred; and (4) for the relief of perigastric 
adhesions, and the less common perigastric, subphrenic, or other peri- 
toneal suppurations. 

CARCINOMA OF THE STOMACH. 

Etiology. — Carcinoma of the stomach is somewhat more common in 
males than in females; and occurs especially after the fortieth year (80 
per cent, of the cases); but it has been observed in subjects less than 
twenty-five years of age, and rarely even in children. The etiological 
factors are the same as those of carcinoma in general, and are as ill 
understood. Some influence is attributed to heredity. The affection is 
more common in the white race than in the negro, and in some 
countries (England) rather than others (America). A history of a 
previous ulcer may be obtained in some cases. 

Pathology.— Carcinoma may involve any part of the stomach, even 
the entire organ, but the lesser curvature and the pylorus are the favorite 
seats. Welch's analysis of 1300 cases showed the pylorus to be the 
seat in 791 (60.8 per cent.), the lesser curvature in 148 (11.4 per cent.), 
the cardia in 104 (8 per cent.), the posterior wall in 68 (5.2 per cent.), 
the whole or greater part of the stomach in 61 (4.7 per cent.), the greater 
curvature in 34 (2.6 per cent.), the anterior wall in 30 (2.3 per cent.), 
the fundus in 19 (1.5 per cent.), and multiple tumors in 45 (3.5 per cent.). 
The carcinoma develops from the mucous membrane, and, as a rule, 
speedily involves the submucous and even the muscular and the serous 
coats of the stomach, and it may spread to adjacent tissues and give rise 
to metastases. The primary growth varies much in size in different 
cases — from a small tumor, 2 to 3 cm. in diameter, to involvement 
of the entire stomach. It may appear as an annular growth about the 
pylorus; as a circumscribed flat elevation, round, ovoid, or irregular in 
outline; as a more or less exuberant cauliflower or polypoid growth 
prone to necrosis; or as a diffuse infiltration of almost if not all of the 
stomach. Extension to adjacent tissues by continuity of structure may 
ensue; and metastases (usually by way of the lymphatics) to the liver, 
regional lymph nodes, omentum, and to more distant organs, occur 
frequently. Welch's analysis of 1574 cases showed metastasis to the 
lymph nodes in 551 cases, to the liver in 475, to the peritoneum, omen- 
tum, and intestine in 357, to the pancreas in 122, to the pleura and lung 
in 98, to the spleen in 26, to the brain and meninges in 9, and to other 



CARCINOMA OF THE STOMACH 639 

parts of the body in 92. Necrosis and ulceration are common. Por- 
tions of the growth may be found in the vomit, and, being subjected to 
microscopic examination, facilitate the diagnosis in a doubtful case. 
Perforation occurs in 4 per cent, of the cases, but it is usually preceded 
and frequently prevented by dense adhesions that bind the stomach to 
the liver, gall-bladder, colon, abdominal wall, etc. In one of my cases 
a large portion (about 10 cm. in diameter) of what at first appeared to 
be the wall of the stomach was made up of the ulcerating and necrotic 
left lobe of the liver — the stomach wall at this place having entirely 
disappeared. Rarely fistulous communications between the stomach 
and the intestines, lungs, pleura, the exterior, etc., may become estab- 
lished. In carcinoma of the pylorus with annular constriction the 
stomach is usually dilated from obstruction, and in some cases it is 
much distorted and displaced; in diffuse carcinoma the stomach wall 
may be greatly thickened and the organ reduced in capacity; whereas 
in carcinoma of the cardia the esophagus is usually dilated and the 
stomach sometimes atrophied. 

The common carcinoma of the stomach is the cylindrical-cell epi- 
thelioma, which may be of the scirrhus, medullary, or colloid variety. 
The so-called malignant adenoma (adenocarcinoma), or adenoma 
destruens, is less common; and the squamous epithelioma occurring 
at the cardia, and usually associated with carcinoma of the esophagus, 
is the rarest. Scirrhus carcinoma may involve the pylorus, causing 
an annular constriction and consequent dilatation of the stomach, or 
it may involve almost if not quite all of the stomach, causing an appear- 
ance much resembling sclerosis of the stomach and exhibiting little 
tendency toward ulceration. Medullary carcinoma occurs as a soft 
cauliflower-like mass that grows with rapidity and commonly ulcerates, 
causing hemorrhage, and may give rise to perforation. Colloid (or 
mucoid) carcinoma occurs as a more or less diffusely infiltrating gela- 
tinous mass that grows with rapidity and involves all the coats of the 
stomach. Malignant adenoma for a time presents a fairly typical 
histological appearance, but exhibits malignant characteristics by its 
diffusely infiltrating tendencies. Secondary carcinoma of the stomach 
has been observed, but is rare. 

Symptoms. — The symptoms of carcinoma of the stomach vary much in 
different cases. Several of the most extensive carcinomas of the stomach 
that I have seen gave rise to no suggestive symptoms during the life 
of the patient, and this latency is by no means uncommon. In other 
cases the symptoms suggest and are sometimes mistaken for pernicious 
anemia; or secondary manifestations, metastases in the liver, superficial 
lymph nodes, etc., attract attention, and the primary growth is overlooked. 
In the majority of cases, however, the diagnosis is readily made, although 
not always in the early stages. In many cases evidences of chronic 
gastritis precede and they usually accompany the symptoms character- 
istic of carcinoma. In Osier's series of 150 cases the symptoms at the 
onset were: Pain in 48, dyspepsia in 44, vomiting in 21, loss of weight in 



640 DISEASES OF THE STOMACH 

13, difficulty in swallowing in 3, and tumor in 1; in 7 the symptoms 
suggested pernicious anemia, and in 37 the onset was acute. The most 
suggestive symptoms are chronic indigestion with persistent epigastric 
pain, and loss of weight and strength, occurring in a person past middle 
life. The epigastric pain is burning or gnawing in character, often 
severe, more or less constant, frequently increased by food (sometimes 
not for several hours), and may radiate to the back or shoulders. Anor- 
exia, nausea, vomiting, and constipation are features of almost all cases, 
but they may be missed. In the early stages the vomiting is not marked, 
but later, especially if either orifice is involved, it becomes a conspicuous 
symptom and may recur several times a day. In carcinoma of the pylorus 
the vomiting may be delayed for several hours after the taking of food; in 
carcinoma of the cardia it usually occurs soon; whereas in carcinoma of 
the body of the stomach it may occur rarely if at all. The vomited 
matter varies somewhat in different cases. If there be associated dilata- 
tion of the stomach the vomit partakes of the characteristics of this 
condition. Usually it consists of undigested, or partially digested, and 
often fermenting foods, mucus, and sometimes blood. Blood occurs in 
one-half or more of the cases. In most cases the blood is small in amount, 
and partakes of the general characters of coffee grounds — the result of 
the action of the gastric juice on the hemoglobin. In some cases the 
hemorrhage is profuse and the blood as ejected is either bright red or 
dark red and clotted, depending upon the length of time it has remained 
in the stomach. Blood may also appear in the stools, with or without 
associated hematemesis. 

The loss of weight and strength, while in the main progressive, is 
subject to interruptions — marked temporary improvement often attend- 
ing the removal of the patient to a hospital, the advent of a new physi- 
cian, regulation of the diet, attention to the appetite, and treatment of the 
co-existing gastritis. Well-marked anemia is a prominent feature of the 
disease and usually progresses concurrently with the loss of weight; 
but it is sometimes so extreme and disproportionate to the other features 
of the disease as to suggest pernicious anemia. Usually, however, the 
blood is of the chloranemic type — the erythrocytes 2,500,000 to 3,500,000 
(being rarely less than 2,000,000, as is common in pernicious anemia) ; 
the hemoglobin varies, but in well-marked cases it is less than 50 per 
cent.; and the leukocytes are sometimes slightly increased, 12,000 to 
18,000. The anemia, emaciation, prostration, and certain attendant 
phenomena, such as a peculiar sallowness and sometimes pigmenta- 
tion of the skin, a distressed countenance, etc., comprise the well-known 
cachexia. In some cases there is slight irregular fever (101° R), attrib- 
utable to the anemia or to infection and suppuration about the car- 
cinoma. 

Examination of the abdomen reveals a visible and palpable mass in at 
least 80 per cent, of the cases some time during their course. This varies 
much in position in different cases, but is usually in the epigastrium, 
hard, nodular, and tender. In many cases, especially if it has formed 



CARCINOMA OF THE STOMACH 641 

adhesions with the liver or gall-bladder, it descends on inspiration, and 
it is often extremely mobile, susceptible of displacement over a wide area. 
On account of the anatomical conditions, as a rule, only tumors of the 
pyloric end of the stomach are palpable. In some cases, especially of 
pyloric obstruction, visible peristalsis may be apparent, or if the tumor 
sufficiently large or the patient sufficiently emaciated, a pulsation be 
transmitted from the aorta may be visible. 

Examination of an Ewald test breakfast reveals absence of free hydro- 
chloric acid in a large proportion (90 per cent.) of cases, and diminution 
in the amount of combined hydrochloric acid; but the total acidity, 
attributable to aromatic (lactic and other) acids, is often high. The 
presence of lactic acid, especially following preliminary lavage and a Boas' 
test meal, possesses much diagnostic value. The presence of a consider- 
able or normal amount of free hydrochloric acid in the presence of symp- 
toms suggesting carcinoma is sometimes believed to indicate ulcus carcino- 
matosum. Microscopicly the most important ingredients of the gastric 
contents are undigested food, yeast fungi, sarcinse, blood (corpuscular 
or crystalline forms), and the Oppler-Boas bacillus — a long non-motile 
organism, usually of much diagnostic value, and answerable for the 
formation of the lactic acid. The milk-curdling ferment is usually 
reduced in amount, and the motor power of the stomach is deficient. 
The stools may contain large numbers of Gram-positive (Oppler-Boas) 
bacilli, in contrast to other conditions in which the stools are Gram- 
negative. 

As the disease advances cachexia increases and metastatic nodules 
develop in different organs. Some of these are accessible to clinical 
observation and sometimes give a clue to the diagnosis — thus nodules in 
the liver, about the umbilicus, or in the left supraclavicular lymph nodes 
just external to the attachment of the sternomastoid muscle, etc. Perfora- 
tion of the wall of the stomach with consequent peritonitis, or fistulous 
communications with different organs, may occur. Ascites due to carci- 
nomatous involvement of the peritoneum or to compression of the portal 
vein by enlarged lymph nodes, jaundice due to obstruction of the bile 
ducts, and oedema of the legs due to anemia or thrombosis of the veins, 
may develop. 

Diagnosis. — In the early stages the diagnosis is often in doubt, but 
chronic indigestion, persistent epigastric pain, loss of flesh and strength, 
absence of free hydrochloric acid and the presence of lactic acid in a test 
meal, occurring in a person past middle life, are extremely suggestive of 
carcinoma. After the occurrence of hematemesis and a palpable tumor 
the diagnosis is no longer in doubt; but at this time the disease has 
advanced to such a stage that hope of lasting benefit can no longer be 
entertained : the growth has made much local progress, and metastases 
undoubtedly have occurred. Chronic gastritis may be distinguished by 
the absence of cachexia, of profound anemia, of leukocytosis, and of 
lactic acid, the presence of free hydrochloric acid (although it may be 
temporarily absent), and the persisting improvement following treat- 
41 



642 DISEASES OF THE STOMACH 

ment. Gastric ulcer may usually be distinguished by its occurrence in 
younger subjects, by gastralgic paroxysms (pylorospasm), epigastric pain 
often augmented immediately by taking food and relieved by vomiting, 
persistent hyperchlorhydria, often profuse hematemesis (occurring in 
apparent health, as contrasted with the hematemesis of carcinoma which 
occurs in weakened and emaciated subjects), absence of cachexia, and 
absence of tumor (although it is sometimes almost if not quite impossible 
to differentiate between the induration and cicatrization of an ulcer and a 
carcinoma). Pernicious anemia may usually be excluded by the predom- 
inance of the gastric symptoms; by the fact that the erythrocyte count 
is rarely less than 2,000,000, and there may be a slight leukocytosis; 
and the characteristic blood picture of pernicious anemia (megalocytes, 
megaloblasts, etc.) is absent. Hypertrophic stenosis of the pylorus 
sometimes gives rise to confusion because of a mass in the epigastrium, 
but it occurs in younger subjects, there is no cachexia and no hema- 
temesis, and the free hydrochloric acid is normal or increased. A gas- 
trocolic fistula is suggested by fecal vomiting and the passage through 
the rectum of unaltered food; but fecal vomiting may be due to reversed 
peristalsis, and an extremely foul vomiting, scarcely to be distinguished 
from fecal vomiting, may be due to ulceration or gangrene of the 
carcinoma. 

Prognosis. — Carcinoma of the stomach leads inevitably to a fatal 
termination — usually within a year from the time the disease is recog- 
nized. Some patients die within three months, and occasionally a 
patient lives two years from the time the disease is recognized. 

Treatment. — The physician's chief concern, since he is unable to cure 
carcinoma of the stomach, should be to recognize it at the earliest pos- 
sible-moment, in the hope that prompt resort to surgical intervention 
may prove of lasting benefit. And since it is impossible in most cases to 
diagnose the disorder until such time that all hope of permanent relief 
has passed, he should suspect it in all cases of persisting indigestion, 
with lessened or absent hydrochloric acid and loss of flesh and strength, 
occurring especially about the fortieth year. In these cases, unless some 
other organic disorder can be found to explain the symptoms, the physi- 
cian should advise an exploratory operation. This will enable the sur- 
geon to make a positive diagnosis, and should the condition prove to be 
carcinoma, operation may be undertaken at a time when hope of success 
can be reasonably entertained. Aside from operative intervention, we 
are limited to relieving the patient's suffering, to feeding him, and pro- 
longing his life. In many cases milk is the best diet; in other cases a 
mixed diet — milk, animal, and vegetable. Lavage is serviceable in per- 
sistent vomiting and in pyloric obstruction. Pain must be relieved by 
external applications, and by the internal use of alkalies, lime water, 
codeine, cocaine, morphine, or cannabis indica, and by the use of anti- 
fermentatives, such as carbolic acid, creosote, resorcin, salicylic acid, 
bismuth, and hydrochloric acid. The appetite may be stimulated by 
nux vomica and the bitter tonics (gentian, quassia, condurango, etc.). 



DISEASES OF THE INTESTINE 643 



NON-CARCINOMATOUS TUMORS. 

Non-carcinomatous tumors of the stomach are rare and of pathological 
rather than clinical interest. Lipomas, fibromas, leiomyomas, sarcomas, 
cysts, and polyps (poly adenomas) have been described. Foreign bodies, 
of which the most curious and remarkable are hair balls, or hair tumors, 
occurring in hysterical women, have been mistaken for carcinoma. 

HYPERTROPHIC STENOSIS OF THE PYLORUS. 

Hypertrophic stenosis of the pylorus may occur as a congenital or an 
acquired condition. The congenital cases are sometimes due to ulcer- 
ation or fissures at the pylorus; in other cases there seems to be only a 
spasmodic contraction of the pylorus (Thomson). The acquired cases 
consist of hyperplasia of the submucous and muscular coats of the 
pylorus. Some of these cases are perhaps developed upon a congenital 
basis, since they become manifest in adolescence. The symptoms consist 
of pylorospasm, pyloric obstruction, consequent dilatation of the stomach, 
and vomiting. In some cases there is visible peristalsis and a palpable 
mass. Some of the cases of periodic or cyclic vomiting in infants and 
children are believed to be due to this hypertrophic stenosis of the pylorus, 
and the associated diaceturia to be the result of starvation. In the mild 
cases, particularly those occurring in infants and children, benefit and 
often cure follows regulation of the diet, especially small amounts at 
frequent intervals of a bland and alkaline diet, and the use of alkalies and 
sedatives, such as the bromides, etc. In some cases resort must be had 
to operative intervention — dilatation of the pylorus, Loretta's operation, 
gastro-enterostomy, etc. 



DISEASES OF THE INTESTINE. 

Pathological Physiology. — The small intestine is designed for the 
further digestion of the chyme received from the stomach and for the 
absorption of the final products of this digestion. In the first portion 
of the duodenum the chyme is still acid in reaction (free hydrochloric 
acid) — which is undoubtedly one reason why the peptic ulcer of the 
duodenum is almost always found in close proximity to the pylorus. 
Lower down the acid chyme encounters and is rendered alkaline and 
otherwise acted upon by the bile and the pancreatic juice. Bile, of 
course, is secreted more or less continuously, but when the stomach is 
empty (that is, during the periods between digestion) it backs up in the 
gall-bladder, largely on account of closure of the sphincter at the end of 
the common bile duct. The stimulus to the discharge of bile into the 
duodenum seems to be proteins and fats, or some of their digestive 



644 DISEASES OF THE INTESTINE 

products; acids, alkalies, and starches are ineffective (Bruns). There 
is some reason, however, to believe that the secretion of bile may be 
stimulated, as is the pancreatic juice, by secretin. The proteins and 
fats entering the duodenum, excite, probably by a reflex action, a con- 
traction of the gall-bladder, and an inhibition of the sphincter closing 
the opening into the intestine (Howell). Bile is both an excretion and 
a secretion. As an excretion it serves to eliminate some end-products 
of katabolism, such as cholesterin, lecithin, bile acids, and bile pigments; 
the bile acids and the bile pigments, however, may be in part reabsorbed. 
The chief action of the bile as a secretion is exerted in the breaking 
up and the absorption of fats. On account of its contained bile acids 
it serves as a medium for the suspension and splitting up of fats into 
fatty acids and glycerin, a hydrolysis effected by the lipase of the pan- 
creatic juice materially aided by the bile. When bile is absent from 
the intestine the fat in the feces is greatly increased (from the normal 
7 to 10 per cent, to as much as 80 per cent.); this is, in part, the cause of 
the pale color of the feces in jaundice, and it suggests the wisdom of 
withholding fats from the feces in such cases. The bile also serves to 
neutralize the acidity of the gastric chyme ard thus enable the trypsin 
of the pancreatic juice to act, trypsin being active only in an alkaline 
medium. Formerly the bile was supposed to exert an antiseptic action 
in the intestine, preventing putrefaction; but these is little real proof 
of this (the bile acts as a good culture medium for bacteria); its absence 
may permit of the putrefaction of proteins and fats which, were the bile 
present, would not occur. The bile was also thought to stimulate 
peristalsis, and to its absence the constipation of jaundice was attributed; 
but there is some doubt regarding the stimulating effect of the bile on 
peristalsis, and constipation is not always present in jaundice. 

The secretion of the pancreatic juice is called forth by a chemical 
stimulus exerted by the acid chyme on the duodenal mucosa; this results 
in the production of a substance, secretin, the consequence of activation 
of an antecedent substance (prosecretin) by the acid of the gastric juice. 
Secretin is absorbed by the blood and carried to the pancreas, where, 
acting as a hormone, it stimulates the pancreas to activity. There is 
some reason to believe that other substances, fats, for instance, may 
act as the efficient stimulus, since the pancreatic juice seems to be 
secreted even in cases in which hydrochloric acid may be absent from 
the gastric juice. 

The pancreatic juice contains three enzymes: (1) Trypsin, a pro- 
teolytic enzyme, which, however, is secreted by the pancreas as trypsin- 
ogen and is activated, converted into trypsin, by enterokinase, a product 
of the intestinal mucosa and a constituent of the intestinal juice. (2) 
Amylopsin (amylase), a diastatic enzyme, the action of which is similar 
to, if not identical with, that of ptyalin of the saliva; it serves to complete 
the digestion of starches. (3) Steapsin (lipase), a fat-splitting enzyme. 
Absence of pancreatic juice from the intestine results in deficient pro- 
teolysis and fat-splitting. The deficient fat-splitting leads to the occur- 



DISEASES OF THE INTESTINE 645 

rence of large, pale, grayish, slate-colored, or clay-colored, pasty, fetid, 
acid stools — which are quite characteristic. 

The intestinal juice (succus entericus) also is active in digestive 
processes; but more so certain enzymes resident in the cells of the in- 
testinal mucosa. These enzymes perhaps may be secreted into the 
intestinal juice, but some of them doubtless exert their activity within 
the epithelial cells themselves. These enzymes are: secretin, the 
hormone stimulating the pancreas to activity; enterokinase, which 
activates the trypsinogen of the pancreas, and forms the proteolytic 
ferment trypsin; erepsin, also a proteolytic enzyme, believed to assist 
in tryptic digestion; nuclease, an enzyme believed to aid in the digestion 
of nucleins; and certain inverting enzymes (maltase, invertase, and 
lactase) that connect disaccharids (maltose, saccharose, and lactose) 
into monosaccharids (dextrose, levulose, and galactose). 

The stimulus calling forth the secretion of this succus entericus is 
not definitely known; it has been attributed to secretin and to the 
mechanical influence of the food. Mechanical and other irritants, such 
as mercury, arsenic, Bacillus dysenterise, saline cathartics, etc., induce 
a watery secretion, that differs materially from the normal intestinal 
juice; a similar watery secretion occurs in chronic passive congestion 
of the intestine, amyloid disease, etc. 

The intestine always contain more or less gases, especially nitrogen, 
derived, in part, from the swallowed atmosphere, in part from bacterial 
decomposition of proteins; carbon dioxide, from carbohydrate fermenta- 
tion and the interaction of the gastric acids on the alkaline hepatic, 
pancreatic, and intestinal secretions; and hydrogen, sulphuretted 
hydrogen, and marsh gas, largely from the putrefaction of proteins. 

The intestinal contents are passed along by peristaltic movements, 
which consist of contractions moving on from segment to segment, 
while the part first contracted gradually relaxes. In addition, there are 
movements of rhythmical segmentation, which have been well studied by 
Cannon, and seem to subserve the purpose of thorough and intimate 
mixing of the intestinal contents. The intestinal movements are not 
continuously progressive from the beginning to the end of the intestine, 
but segmental and pendulum-like, though ultimately they serve to 
pass the intestinal contents onward. Readily digestible food appears 
to traverse the small intestine in about four hours, and to reach the sig- 
moid colon in two or three hours more (Hertz). Exaggeration of the 
intestinal movements gives rise to borborygmi, which is especially 
marked when the intestine contains much gas and little food. Exagger- 
ated contractions against a mechanical obstruction or incoordinated 
contraction and relaxation give rise to intestinal colic; stimulation of 
the splanchnics (through which a nervous control is exerted) may cause 
colic and constipation (as in lead poisoning); and paresis or paralysis 
may lead to a form of nervous diarrhoea. Antiperistalsis does not occur 
in health, but may be observed in diseased conditions, especially those 
attended by intestinal obstruction. 



646 DISEASES OF THE INTESTINE 

The function of the large intestine is largely to absorb water from 
the intestinal contents, and thus indirectly to cause inspissation of the 
intestinal contents. Very little nutritive matter is absorbed by the colon, 
so that persons fed by rectal alimentation soon begin to suffer from 
starvation. 

In health, divers sorts of bacteria are found in the intestinal tract, 
especially in the large bowel, notably Bacillus coli; in disease the number 
of species may become increased, or the normal inhabitants may be over- 
come by the invaders. Zooparasites also are common. It seems likely 
that bacterial activity is of much importance in the orderly performance 
of the intestinal functions, and that derangements of this bacterial 
activity may lead to diseased processes. Those to which chief importance 
is attached are associated with putrefactive changes; the disorders to 
which they are supposed to give rise are called intestinal auto-intoxica- 
tions, which have already been discussed (page 303). 

The feces consist of: (1) Indigestible material (ligaments of meat, 
cellulose from vegetables); (2) undigested material, such as fragments 
of meat, starch, or fats which have escaped digestion; (3) products of 
intestinal secretions; (4) products of bacterial growth, especially indol 
and skatol, to which the odor of the feces is largely due; (5) cholesterin, 
probably derived from the bile; (6) purin bases, especially guanin and 
adenin; (7) mucus and epithelial cells thrown off from the intestinal 
wall; (8) pigment, especially urobilin or stercobilin, derived from the 
bilirubin of the bile; (9) inorganic salts — salts of sodium, potassium, 
calcium, magnesium, and iron, chiefly the last three together with 
phosphoric acid; and (10) microorganisms, usually in great quantities 
(Howell). Study of the feces is of much importance in determining 
the functional efficiency of the intestines. This is best done after the 
use for three or more days of Schmidt's test diet (see intestinal indi- 
gestion). 

SYMPTOMATIC DISORDERS OF THE INTESTINE. 

Disorders of the functions of the intestine are the natural consequence 
of definite anatomical lesions of most diverse nature, and as such are 
usually recognized and correctly ascribed to a more or less obvious 
cause. In other cases intestinal symptoms are due to, or part and 
parcel of, a general neurosis, such as hysteria, neurasthenia, etc. , or they 
are reflex manifestations of disease of some adjacent viscera; whereas in 
other cases the intestinal disorder seems to be due entirely to some per- 
version of the functional activity of the intestinal nervous mechanism, 
and is unassociated with discoverable anatomical lesions ; in other words, 
the condition is a neurosis. The dividing line between these different 
classes of cases, however, is by no means distinct, and sometimes cannot 
be drawn at all. We may, nevertheless, as in the stomach, distinguish 
disorders of motility, of sensibility, and of secretion, though they often 
do not occur alone. 






SYMPTOMATIC DISORDERS OF THE INTESTINE 647 

Motor Disorders. — Disorders of motility are dependent upon in- 
creased or decreased irritability of the motor nerves and musculature: 
on the one hand, peristaltic unrest, nervous diarrhoea, or enterospasm, 
results; on the other hand, paresis or paralysis. 

Peristaltic unrest (intestinal tormina), a condition allied to peristaltic 
unrest of the stomach, is not infrequently a manifestation of catarrhal 
enteritis or intestinal stenosis, but it sometimes occurs also as an appa- 
rently independent affection, especially in nervous, hysterical, and 
hypochondriacal women, and rarely even in persons without other neuro- 
pathic manifestations. The condition consists of rolling and gurgling 
sounds in the intestine, varying much in intensity from time to time, 
sometimes so loud as to be audible some considerable distance from the 
patient, and often occasioning extreme annoyance and discomfort, 
especially when they are, as sometimes, loud and squeaking. Pain is 
rarely complained of. The condition is due to increased peristalsis of the 
small intestine carrying along the gaseous and fluid contents from one 
segment of the intestine to another. Eructations may occur in associated 
peristaltic unrest of the stomach, and Rosenheim even reports feculent 
vomiting (which, however, must be exceedingly rare). The peristaltic 
movements are not infrequently visible and even palpable through thin 
abdominal walls. The attacks usually come on without notewor hy 
cause, though they may be provoked by emotional disturbances, certain 
articles of diet, etc.; they usually last for a few minutes, though some- 
times for hours, and even during sleep; and they occur at irregular 
intervals. 

Nervous diarrhoea is a condition dependent upon increased peri- 
staltic movements, on the one hand, and an increased transudation of 
fluid into the intestine, on the other hand. Allied in some respects to 
peristaltic unrest, it differs in that, in at least some cases, the increased 
peristalsis seems to be almost, if not wholly, limited to the large intes- 
tine (whence the intestinal evacuations), and in the rapid transudation of 
fluid. This is certainly attributable to nervous influences (paresis or 
paralysis of the splanchnics) — since there is no other evidence of disease 
of the intestine, and the attack is almost always provoked by emotional 
disturbances, such as shock (unwelcome news), fright, ordeal of the 
witness stand, public speaking, examinations (students, etc.). A similar 
condition is sometimes observed in nervous disorders like tabes, and may 
occur as a reflex manifestation in different gastro-intestinal disorders, 
disorders of the female genitalia, e c. The stools vary in number from 
three or four to a dozen or more, are often passed in rapid succession, 
and consist of thin liquid material. Sometimes the first evacuation is 
of more or less well-formed fecal matter, whereas the subsequent stools 
are very thin and serous. Peristaltic unrest (rolling and gurgling sounds) 
sometimes accompanies the evacuations. A somewhat similar condition 
is occasionally observed in persons generally constipated, who when they 
become "nervous" from any cause, have an almost immediate evacuation 
of the bowels. Diarrhoea is also a common symptom of many diseases 



648 DISEASES OF THE INTESTINE 

of the intestine, notably acute and chronic enteritis, under which head- 
ings it is discussed. 

Spasm of the intestine (enterospasm) is a term applied to tonic con- 
tracture of the muscular fibers (longitudinal and circular) of the intes- 
tine, resulting in lessening or complete though temporary occlusion of 
the lumen. The very rare occurrence of a primary or idiopathic entero- 
spasm may be conceded, the subjects being neuropathic or hysterical 
individuals; the condition, however, is almost always secondary or 
symptomatic. It may be a manifestation of local inflammatory or other 
diseases of the intestine; it is a common manifestation of lead intoxication; 
and is not uncommon in diseases of the brain, especially meningitis, 
in which the intestinal contractures may be associated with scaphoid 
retraction of the abdomen. The spasm may be more or less diffuse, 
involving large sections of the small or large intestine, or both; or it may 
be quite circumscribed — of which variety, proctospasm (usually asso- 
ciated with other diseases of the rectum or anus) is a well-known 
example. Clinically the condition resembles enteralgia (of which it is 
really often the anatomical basis), and constipation is common; but 
neither pain nor constipation is essential. Local tympany or meteorism 
is not infrequent. When confined to the lower bowel, the feces may be 
narrow or ribbon-like, or resemble sheep's dung. 

Paralysis of the intestine may be due to a variety of causes. It is 
common in peritonitis from whatever cause arisen; it may be a concomi- 
tant of intestinal obstruction; it is associated with a form of chronic 
atony with consequent constipation; and it is sometimes observed in 
hysterical subjects who suffer much from meteorism. Constipation is the 
conspicuous clinical feature. Paralysis of the anal sphincter is found in 
divers disorders of the brain associated with stupor and coma, especially 
infectious diseases like typhoid fever, various intoxications, and more 
purely local diseases of the brain associated with coma; it is a charac- 
teristic symptom of certain organic diseases of the spinal cord; and it 
sometimes develops after the persistence of irritating diseases of the 
rectum associated with long-standing tenesmus which ultimately leads to 
fatigue, paresis, and paralysis of the muscles. Paresis usually precedes 
paralysis, so that at first the patient by an effort can control the evacua- 
tions; later, the slightest disturbance or undue pressure results in the 
discharge of gas or fecal matter; and ultimately, when paralysis is com- 
plete, the intestinal contents are altogether beyond the control of the 
patient and may be discharged immediately they enter the rectum. 

Treatment. — The treatment of the motor disorders of the intestine is 
similar to that of similar disorders of the stomach. Especial attention 
should be directed to the underlying conditions, whether neuropathic 
or local anatomical factors that may determine the onset, or augment 
an attack. The diet must be regulated and the bowels must be opened 
regularly and daily. Hydrotherapeutic measures, electricity, a course 
of treatment at certain health resorts, etc., are of benefit in many 
cases. Drugs, such as arsenic and the bromides, and sometimes strych- 



SYMPTOMATIC DISORDERS OF THE INTESTINE 649 

nine and iron (in anemic conditions), may subserve a useful purpose. 
Belladonna or hyoscyamus may be useful in spasm; and physostigma 
or eserine may be useful in overcoming constipation due to atony. 

Sensory Disorders. — The sensibility of the intestinal tract may be 
increased (hyperesthesia, pain), diminished (anesthesia), or perverted 
(paresthesia). 

Intestinal pain (enter odynia) may be due to one of several causes : (1) 
It may be a manifestation of inflammation of any portion of the intestine 
and of its peritoneal covering (to be discussed under appropriate head- 
ings). (2) It may be the so-called intestinal colic. (3) It maybe a true 
intestinal neuralgia. 

Intestinal colic, the pain produced by violent tetanic contractions of 
the muscular coat of the intestine, may be due to : (1) Sudden chilling 
of the surface of the body, which of itself seems to provoke intestinal 
colic in certain susceptible persons; (2) dietetic indiscretions — coarse, 
indigestible, unripe, or decomposed food, especially unripe fruit and 
overripe fish, and cold drinks; (3) foreign bodies, such as gallstones, 
enteroliths, scybalous masses, large amounts of mucus (mucous colic), 
etc.; (4) drastic cathartics and other medicines; (5) infections and 
intoxications, such as certain infectious diseases (cholera), lead poisoning, 
etc.; (6) zooparasite invasions, intestinal worms; (7) reflex disturbances 
associated with disease of the ovaries, uterus, bladder, kidneys, etc. 

Intestinal colic usually comes on suddenly with severe pain radiating 
in different directions (though it may remain localized) ; it varies much 
in intensity (from moderately severe "griping" to extremely severe 
pains), remits and intermits, and varies in duration from a few 
moments to several hours. Nausea, vomiting, flatulence, and faint- 
ness are not uncommon; if the pain is severe, cold perspiration 
usually breaks out; and exhaustion and collapse may supervene. The 
attack usually subsides with the removal of the exciting cause, often with 
the discharge of feces (stercoral colic), sometimes with the evacuation 
of gas (flatulent colic), or of mucus (mucous colic). 

Intestinal colic may simulate hepatic and renal colic in the sudden 
onset and sudden cessation, as well as severity, of the pain, but in 
hepatic colic the pain is usually referred to the right hypochondrium, 
and may be referred to the right shoulder; it is not so likely to be inter- 
mittent; jaundice and bile-stained urine may occur; there may be a 
history of similar attacks; and gallstones may be found in the feces. 
In renal colic the pain is usually in the back, loin, or groin, and 
radiates to the testicle, which may be retracted; strangury or frequent 
micturition is common, the urine may become bloody, and a calculus 
may be found in the urine. 

The term intestinal neuralgia, or nervous enteralgia, may be applied 
to attacks of abdominal pain, seen in nervous, hysterical, and hypo- 
chondriacal women (rarely men), which come on suddenly, spread 
usually from the umbilicus over the abdomen, last a variable time 
are likely to recur, and seem to be unusual in severity, leading fre- 



650 DISEASES OF THE INTESTINE 

quently to collapse, and in which there is no etiological or other evidence 
of true intestinal colic, nor of inflammation of the abdominal viscera or 
peritoneum. Vomiting is absent, the stomach and intestines perform 
their functions normally; but cutaneous hyperesthesia and other evi- 
dence of hysteria, etc., are present. In the absence of better knowledge, 
the condition is described as a neurosis — a neuralgia of the mesenteric 
plexus and the splanchnic nerves; but in some cases, as for instance 
the crises and other perhaps analogous conditions, the pain is doubtless 
due to angiospasm. 

Diminished sensibility (anesthesia) of the intestine attends and 
may be the cause of constipation. It is found especially in different 
diseases of the brain and spinal cord associated with paralysis, and in 
fecal accumulations. If the motor innervator of the intestine is unim- 
paired, spontaneous evacuations occur, but with defective motility 
constipation, often extremely obstinate, occurs. 

Paresthesia of the intestine is rather unusual, though it may be com- 
plained of by the hysterical and the insane. The paresthetic phenom- 
ena are usually (though not always) referred to the rectum. 

Treatment. — The treatment of the sensory disorders of the intestine 
is determined by the etiological factor. The pain may be relieved by 
hot applications to the abdomen — poultices, hot-water bag, mustard 
plaster, spice poultice, turpentine stupe, and by the internal administra- 
tion of spirit of ginger, aromatic spirit of ammonia, compound spirit of 
ether, camphor, chloroform water, or a dry Martini cocktail (the one 
instance in which it subserves a very useful purpose). Rarely morphine 
or other preparations of opium must be resorted to. The bowel should 
be evacuated immediately by rectal enemas, and by castor oil by the 
mouth. Subsequently attention must be directed to the diet, to regu- 
larity in the movement of the bowels, and to the underlying general 
condition. Tonics, stimulants, and other measures mentioned under 
constipation (page 656) are sometimes necessary to overcome the con- 
stipation due to diminished sensibility; in some cases manual removal 
of the feces may have to be resorted to. 

Secretory Disorders. — The intestinal juice under the influence of 
the nervous system is subject to increase and decrease — depending 
upon a variety of factors. Diminution is doubtless a factor in some 
cases of constipation; increase is an important factor in so-called 
nervous diarrhoea, in which the evacuated fluid is largely serous in 
character; but the only disease described as wholly or almost wholly a 
secretory disorder or neurosis is so-called mucous colic or colitis. 

INTESTINAL INDIGESTION. 

{Intestinal Dyspepsia; Dystrypsia.) 

In health the entrance of the chyme into the duodenum, by activat- 
ing the prosecretin of the duodenal mucosa and thus forming secretin, 
gives rise to the secretion of bile and of pancreatic juice which not only 



INTESTINAL INDIGESTION 651 

neutralize the acidity of the chyme, but also produce that alkalinity 
required for the proper digestive activity of the ferments contained in 
these juices. Intestinal digestion then depends not only upon the proper 
amount of bile and of pancreatic juice of good quality, as well as of 
intestinal juice, but also upon the functional integrity of the stomach: 
since defective gastric digestion not only results in the introduction into 
the duodenum of chyme ill adapted to the intestinal functions, but defi- 
cient or increased acidity results in corresponding derangement of the 
flow of bile and of pancreatic juice into the intestine — though doubtless 
minor deviations from the normal can be compensated for. Intestinal 
indigestion — disorders of the processes of digestion occurring in the 
intestine — may be primary or secondary, although it is often difficult, 
if not impossible to separate the one from the other. 

Etiology .—Primary intestinal indigestion results from: (1) Disease of 
the small intestine, of whatsoever nature, but especially chronic catarrh, 
interfering with the absorptive power of the mucous membrane, as well 
as with the formation of an active intestinal juice. (2) Change in the 
quality or quantity of the bile. A diminished amount of bile may be 
due to sluggish action of the liver or to obstruction to the entrance of 
bile into the intestine arising from any cause whatever. Changes in the 
quality of the bile are ill understood, though it seems that the liver has 
the function of eliminating by way of he bile and the intestine certain 
end products of metabolism, and it is not inconceivable that these in 
excess may interfere with the action of the bile or irritate the intestinal 
mucosa. (3) Changes in the quantity or quality of the pancreatic juice. 
Secondary intestinal indigestion may arise in consequence of any form 
of gastric indigestion — especially gastric hyperacidity, but also subacidity, 
deficient motor power, etc. 

Symptoms. — The symptoms of intestinal indigestion usually accompany 
and sometimes cannot be dissociated from those of gastric indigestion. 
The patient usually complains of loss of appetite, acid eructations, flatu- 
lency, epigastric distress and distention (in consequence of acid fermen- 
tation of carbohydrates, putrefactive decomposition of albuminous 
foodstuffs), and of diarrhoea, the result of irritation and consequent 
increased peristalsis often occasioned by abnormal acidity of the intes- 
tinal contents. The diarrhoea is often and characteristically preceded 
by pain, which may be colicky in nature. The stools at first consist of 
the contents of the lower part of the bowel, but soon present the charac- 
teristics of the contents of the jejunum, being semifluid, gelatinous, and 
tenacious — due to a large amount of mucus, the normal contents of the 
jejunum, and not the result of catarrh (as shown by the absence of 
formed elements, epithelial cells, and round cells so common in catarrh). 
Furthermore, the stools, often yield a pronounced reaction for bile 
(though this, of course, varies with the amount of bile present); they 
are sometimes quite greenish in color, though often light yellowish and 
foamy, and yield an odor of butyric acid. 

The nature of the disorder in protracted cases is best determined by 



652 DISEASES OF THE INTESTINE 

study of the stools after the use for three days or more of Schmidt's test diet. 
This consists of: In the morning, 500 c.c. of milk and 50 grams of Zwie- 
back; in the forenoon, 500 c.c. of oatmeal gruel (made up of 40 grams of 
oatmeal, 10 grams of butter, 200 grams of milk, 300 grams of water, 1 
egg, and some salt); at noon, 125 grams of chopped beef broiled rare, 
with 20 grams of butter, and 250 grams of potato puree (190 grams of 
potatoes, 100 grams of milk, 10 grams of butter, and a little salt); in the 
afternoon, milk and Zwieback, as in the morning; and in the evening, 
oatmeal gruel, as in the forenoon. This diet furnishes about 2250 
calories. Special attention should be paid to the presence in the stool 
of connective tissue, muscle tissue, potato (or starch) granules, fat 
(fatty acids and soaps), mucus, and bacteria. Special importance at- 
taches to the presence of muscle tissue, starch granules, and fatty acids. 
Resort may also be had to Sahli's dermoid test, etc. 

Persistence of the attack soon leads to catarrh of the intestine, and the 
usual catarrhal stools (alkaline reaction, evidences of catarrhal desqua- 
mation, etc.). 

Diagnosis. — The cases due to disorder of the stomach may be distin- 
guished by symptoms especially referable to the stomach, the results of 
analyses of the gastric contents after a Boas or Ewald test meal, the 
presence of much connective tissue in the stools after Schmidt's test diet, 
and improvement following treatment directed to the stomach. 

Treatment. — The treatment consists especially in regulating the diet, 
in accordance with the findings of a gastric analysis and a study of the 
stools. The medicinal measures depend upon the underlying conditions 
and the digestive capacities. Gastric hyperacidity or subacidity calls for 
appropriate treatment. Carminatives and so-called intestinal antiseptics, 
such as resorcin, bismuth salicylate, naphthalene, creosote, carbolic acid, 
aromatic spirit of ammonia, salicylic acid, etc., are usually indicated. 
Calomel in small doses, fa to 2V grain (0.0015 to 0.003 gram) three or 
four times a day, is an excellent remedy in some cases, from time to 
time, although, if it stimulates peristalsis, the dose should be reduced. 



INTESTINAL HEMORRHAGE. 

(Enter orrhagia.) 

Etiology. — Blood issuing from the body by way of the anus may be 
evidence of hemorrhage from any part of the gastrointestinal tract, and 
may be due to many causes — local and general. The general causes are 
such as determine hemorrhage in other parts of the body — purpura, 
scurvy, malignant (or hemorrhagic) forms of certain specific infections 
(smallpox, yellow fever, cholera, malaria, measles, scarlatina, diphtheria, 
etc.), septic infections (malignant endocarditis, etc.), leukemia, perni- 
cious anemia, etc. ; and it is rarely a manifestation of vicarious menstru- 
ation. The local causes are : (a) Hyperemia of the intestine, common in 
advanced cirrhosis of the liver, and in heart disease, less common in the 



INTESTINAL HEMORRHAGE 653 

early stages of acute inflammations, such as typhoid fever, (b) Inflam- 
mation, erosion, and ulceration of the intestine, such as the inflammation 
provoked by irritant poisons or drastic cathartics ; peptic or other ulcera- 
tion of the stomach or duodenum; and the various forms of ulceration 
(simple, tuberculous, syphilitic, carcinomatous, etc.) of other portions 
of the intestine; typhoid fever; dysentery; etc. In some cases even large 
hemorrhages seem to have resulted from mere superficial erosion of the 
mucous membrane, (c) Embolism and thrombosis of the mesentric 
vessels, (d) Changes in the vessel walls, such as occur in amyloid 
disease, nephritis, etc., may occasion hemorrhage — in some cases in 
consequence of the formation and rupture of miliary aneurysms, (e) 
Zooparasite invasion of the intestine, as by Uncinaria duodenalis, 
Schistosoma haematobium, etc. (J) Hemorrhoids, internal and external, 
and anal fistula or fissure, (g) Trauma, external blows, or internal 
injuries provoked by divers kinds of foreign bodies (chicken bones, 
oyster shells, enteroliths, hard feces, etc.). In women, blood supposed 
to issue from the bowels sometimes comes from vaginal sources. In 
addition, blood issuing from the anus may be due to swallowing of 
blood coming from the nose, throat, oesophagus, or lungs (hemoptysis). 

Symptoms. — The symptoms of intestinal hemorrhage vary much 
with the cause and the amount of the hemorrhage. When slight, the 
hemorrhage often passes unnoticed, or may be merely an accidental 
finding in the stool. This is sometimes the case in latent ulceration, 
carcinoma, or parasitic invasion of the intestines (occult blood), and may 
require microscopic or chemical tests for its detection. When large the 
symptoms may be exceedingly severe, and occasionally lead directly to 
death, although as much as two or three quarts may be lost at one time, 
and even a debilitated patient survive (typhoid fever). Sudden large 
hemorrhage is manifested by faintness, dimness of vision, and vertigo, 
often progressing to collapse, pallor of the skin and visible mucous 
membranes, profuse perspiration, and fall of temperature (often 5° to 8° 
or more). Repeated small hemorrhages lead to the gradual develop- 
ment of marked anemia (see chronic secondary anemia, page 367). 

When the blood comes from the stomach or the upper part of the 
intestine it is usually altered by the digestive juices, and issues from 
the anus as black tarry fluid or masses (melena). Very rarely a massive 
hemorrhage coming from the stomach or upper part of the duodenum 
and issuing soon from the anus may be but little altered. Blood coming 
from the lower part of the small bowel, or from the colon or the rectum, 
is comparatively unaltered and readily recognized as blood. Should the 
hemorrhage occur from the stomach, or from the upper part of the intes- 
tine, and the blood find its way into the stomach, hematemesis may 
accompany the enterorrhagia. But very large, and even fatal hemor- 
rhages may occur without any external discharge of the blood. 

Treatment. — The treatment of intestinal hemorrhage is to be based 
entirely upon its source. In general it is similar to that of hemorrhage 
occurring in typhoid fever (page 59). 



654 DISEASES OF THE INTESTINE 

MUCOUS COLIC. 

(Mucous Colitis; Pseudomembranous Enteritis; Tubular Diarrhoea.) 

Mucous colic is a secretory neurosis of the colon characterized by the 
formation of an excessive amount of tough, tenacious mucus. 

Etiology. — Mucous colic is not so rare a disease as was formerly sup- 
posed, and is most common in neurotic and hysterical women (80 per 
cent, of the cases). It is rare in children. In most cases it is an inde- 
pendent disorder, and occurs without noteworthy anatomical lesions in 
the intestinal mucosa. In some cases, however, it seems to become 
engrafted upon an intestinal catarrh; that is, to the catarrhal altera- 
tions are added, either permanently or periodically, the manifestations 
of the neurosis (hypersecretion of mucus). Constipation appears to be a 
contributing etiological factor in some cases. 

Symptoms. — The disease is characterized by the passage from the 
bowel of large amounts of mucus. This occurs usually in paroxysms, 
frequently of unknown cause, but sometimes induced by psychic dis- 
turbances, dietetic indiscretions, and divers extraneous causes. The 
paroxysm is usually attended by severe abdominal pain, which is some- 
times so severe as to suggest to the patient impending dissolution, and 
to engender the morphine habit. The pain is most commonly along the 
course of the descending colon, and is frequently accompanied by 
tenderness. The pain and tenderness, however, may be on the right 
side, and being sometimes associated with palpable tenderness of the 
appendix, suggest an etiological relationship, which seems to be proved 
in some cases by recovery after removal of the appendix. Rarely pain 
is absent. Tenesmus is a distressing feature of some cases. The attack 
may last for from several days to two weeks or longer, but mucus is not 
passed with each paroxysm of even severe pain. The mucus occurs 
as shreds, flakes, narrow cylinders (suggesting certain intestinal worms), 
or sometimes as tubes forming veritable casts of the bowel. Usually the 
stool consists exclusively of this mucus, and a very large amount may be 
passed at one time. As a rule, the mucus is opaque and grayish; occa- 
sionally it is brownish from admixture with feces, and rarely reddish, 
from admixture with blood. Occurring in masses or as casts the mucus 
often resembles fibrinous exudates, but microscopic examination (mucus 
cells, cylindrical epithelial) and chemical examination (mucin reaction) 
reveals it to be composed exclusively of dense, tough, altered mucus. 

As a rule, the patients present the ordinary manifestations of hysteria, 
neurasthen'a, hypochondriasis, etc. Constipation is the rule between 
attacks. The condition lasts for years, and in many cases, ultimately 
leads to marked anemia,and emaciation. 

Treatment. — The treatment is eminently unsatisfactory. During the 
paroxysm measures should be taken to relieve the pain, such as hot 
fomentations to the abdomen, and to get rid of the cause of the pain by a 
thorough evacuation of the bowels — by castor oil and rectal enemas. 



CONSTIPATION 655 

The cure of the disorder comprises attention to the underlying hysteria 
or neurasthenia, rather than measures suggested by a supposed intes- 
tinal catarrh (which is rarely present). Attention to the common con- 
stipation is frequently followed by marked improvement in the mucus 
colic. A right-sided colotomy with maintenance of an artificial anus 
for some time, and consequent rest of the colon, has been successful in 
a few cases. 

CONSTIPATION. 

(Costiveness.) 

Constipation is a condition in which the feces are retained in the 
intestinal canal an unusually long time; as a rule, the feces when 
passed are unduly hard. There may be a daily movement, in which 
event the evacuation is insufficient. 

Etiology. — Constipation may be due to many causes — general and 
local. The general causes comprise family or individual tendency, 
"bad habits" (non response to the calls of nature), sedentary life, die- 
tetic errors (too little food, or foods that leave little residue), habitual 
use of purgatives, certain nervous disorders (such as hysteria and neuras- 
thenia, as well as organic disorders interfering with the evacuation of the 
bowel), hepatic disorders associated with jaundice, acute infectious 
fever, general debility, etc. The local causes are: (1) Diminished 
expulsive power, that is, defective intestinal peristalsis, atony of the 
intestine (itself also a result of chronic constipation), or weakness of 
the diaphragm or the abdominal muscles (obesity, distention from 
repeated pregnancies, etc.); and (2) increased resistance to the onward 
movement of the feces, which may be due to (a) hardness and dryness 
of the feces; (b) lessening of the intestinal lumen from any cause 
(see intestinal obstruction); (c) inhibition of the free movement of 
the intestine in consequence of adhesions or abdominal bands; (d) 
displacement of the intestine (V-shaped colon, redundant sigmoid); 
(e) spasm of the intestine, usually of the lower colon or sigmoid (with 
atony and dilatation of the proximal parts of the intestine) — so-called 
spasmodic constipation, observed especially in hysterical and neuras- 
thenic women, particularly the subjects of ovarian or uterine disease. 

Constipation is symptomatic when due to obvious causes, idiopathic 
when no cause can be ascertained. When symptomatic, it is usually 
more or less temporary; when idiopathic, it is not infrequently a habit — 
so-called habitual constipation. 

Symptoms. — There is marked diversity in the reaction to constipation. 
Many persons are habitually constipated and otherwise apparently well; 
others, occasionally constipated for greater or less periods, suffer little 
discomfort; whereas in others the failure to have the daily evacuation 
produces immediate and notable discomfort, and protracted consti- 
pation brings a long train of symptoms in its wake — copremia (intes- 
tinal auto-intoxication). Most extraordinary cases are occasionally 



656 DISEASES OF THE INTESTINE 

observed — cases in which no evacuation has occurred for weeks and 
even months. 

Although, in many cases, constipation is the only complaint, there is 
often a feeling of discomfort in the rectum. Overloading and conse- 
quent distention of the sigmoid may occasion pain from pressure on 
regional nerves. There is frequently associated flatulence, borborygmi, 
occasional attacks of colicky pain, and diarrhoea (which should not be 
misinterpreted). Hemorrhoids are common; inflammation, dilatation, 
ulceration, and even perforation of the intestine may result; and men- 
struation is likely to be painful. The retained feces usually become 
hardened, in consequence of absorption of the watery constituents, and 
form scybalous masses; these may be palpated through the abdomen 
as irregular, sometimes sausage-shaped tumors, in the course of the 
colon. Occasionally scybalous masses retained in sacculi of the colon 
give rise to the development of enteroliths. In spasmodic constipation 
the fecal discharges may be narrow and ribbon-like, or resemble the 
discharges of sheep. 

In many cases the appetite is lost (or lessened), the tongue coated, 
and the breath foul; headache, vertigo, palpitation of the heart, are not 
uncommon; and depression of spirits, hypochondriasis, etc., are likely 
to supervene. 

Constipation in infants may be congenital, or due to dietetic indis- 
cretions, or to local causes similar to those causing constipation in adults. 
Some infants, constipated from birth, require for months a daily enema 
or aperient to secure an evacuation. Certain artificial foods seem to 
engender constipation in some infants, a deficiency of fat being believed 
to be the active factor. In older children the costive habit is often 
favored by inattention on the part of the mother. 

Treatment. — The cultivation of habits of regularity is of the utmost 
importance, and only those who have observed know the good effects 
that may be thus achieved. The patient should go to stool at the same 
time every day, whether there is a desire to evacuate the bowels or not, 
and every such desire should be immediately gratified. The diet should 
comprise considerable fruit and vegetables (which leave a residue). A 
glassful of cold water before breakfast, an orange or oatmeal at break- 
fast, and stewed fruits and salads at dinner subserve a useful purpose 
in many cases. Persons of sedentary habits are often benefited by exer- 
cise; abdominal massage is useful in some cases; and an abdominal 
binder is of value to those with a pendulous flabby abdomen and 
visceroptosis. 

Drugs should be dispensed with as long as possible. Even in long- 
standing cases much and lasting benefit may be secured by dietetic and 
hygienic measures. Medicinal measures when necessary vary with the 
nature of the causal factor, which must be diligently searched for. At 
the beginning of the treatment it is often advisable to clear the in- 
testine thoroughly with castor oil, a blue mass pill, or calomel, followed 
by a saline aperient. In many cases, the best results are obtained by a 



ACUTE ENTERITIS 657 

daily injection of tepid water with or without soap; in other cases 
injections of oil are much better; but enemas should not be too long 
continued. Some patients are much benefited by a saline aperient 
water, sodium phosphate, or other saline, taken a half hour before 
breakfast. Those who are occasionally constipated, find relief in a 
Seidlitz powder, compound licorice powder, the official compound 
cathartic pill, or a glycerin suppository. Should a course of medicine 
be necessary, the desired results may usually be secured by the use of 
cascara sagrada, which has the advantage that, having been continued 
for some time, the dose necessary to secure a daily evacuation may be 
gradually reduced, and the drug ultimately dispensed with, should the 
patient continue habits of regularity. The pill of aloin (■§■ grain, 0.008 
gram), strychnine (■£$■ grain, 0.0015 gram), and extract of belladonna (^ 
grain, 0.006 gram), though much abused, is very useful in many cases. 
The following pill night and morning is also useful : 

]$— Podophyllin tV to I g rain °| 006 to °- 012 

Strychnine ^g- grain 0'0015 

Ext. physostigma ^ grain 008 

Ext. belladonna ^ grain 0|01 

Instead of the podophyllin, aloin, extract of cascara sagrada, or com- 
pound extract of colocynth may be substituted. Phenolphthalein (1 to 
2 grains, 0.06 to 0.12 gram) at night is often attended by good results. 
Rhubarb and sodium bicarbonate also are of value in some cases. A pill 
of iron (dried sulphate of iron, 2 grains, 0.12 gram) and extract of aloes 
(1 grain, 0.06 gram), with or without rhubarb (5 grains, 0.3 gram), is 
often efficacious in the constipation of anemic and chlorotic conditions. 
Agar-agar (15 to 30 grains, 1 to 2 grams or more) eaten with cream, 
twice or thrice daily, is often serviceable when the feces are hard and 
small in amount. Similar results may be achieved by the use of large 
amounts of fats, olive oil, butter, cream, etc. 

In children the best results follow attention to the diet, the giving 
of cream, barley water, oatmeal water, etc. Rectal injections may be 
required, or a conical piece of soap may be introduced within the anus. 
Among medicines, magnesia, manna, rhubarb and soda, and olive oil are 
probably the best, but if possible all medicine should be avoided. 



ACUTE ENTERITIS. 

(Acute Intestinal Catarrh; Cholera Morbus; Cholera Nostras.) 

Acute enteritis is an acute inflammation of the intestinal mucous 
membrane, characterized by abdominal pain and diarrhoea. 

Etiology. — The affection occurs at all ages, in both sexes, and is 
especially prevalent during the summer months. Its causes are: (1) 
Bacterial infection, which sometimes causes a primary infectious enter- 
itis. An enteritis is common also in many infectious diseases, such as 
typhoid fever, cholera, pneumonia, dysentery, etc. (2) Animal para- 
42 



658 DISEASES OF THE INTESTINE 

sitic infections — worms, etc. (3) Toxic and mechanical irritants, such 
as improper food (tainted meats, overripe or underripe fruit); stomach 
contents improperly prepared for the intestine; intestinal contents that 
remain too long in the intestine (in consequence of stenosis or imperfect 
action of the intestinal musculature); drastic cathartics; irritant poisons; 
certain articles of diet and waters to which the individual may be un- 
accustomed (personal idiosyncrasy), etc. (4) Certain autogenic poisons, 
such as occur in uremia, and which irritate the intestinal mucosa. Second- 
ary enteritis occurs in heart disease and liver disease in consequence of 
passive congestion; in amyloid disease (undue permeability of the 
intestinal bloodvessels), etc. 

Pathology. — The lesions are those of catarrhal inflammation in general 
■ — swelling, hyperemia, and increase of mucous secretion, with des- 
quamation of the surface epithelium. In many cases, however, at the 
necropsy, but few or slight changes may be apparent. Frequently, in 
addition to swelling, there is superficial erosion or ulceration of the 
solitary and agminate lymph follicles (catarrhal and follicular ulcera- 
tion). In severe cases, small hemorrhages in the mucosa may occur 
(hemorrhagic enteritis). The lesions may extend throughout the entire, 
intestinal tract, but are often more marked in one part than another. 

Symptoms. — Diarrhoea may be the only symptom, and even this may 
be inconspicuous in catarrh of the upper part of the small bowel. The 
stools vary much in frequency — four to twenty or more in the twenty- 
four hours; in amount, from small movements to great losses of fluid 
(liters); in color, from dark brownish to light yellowish or grayish, de- 
pending upon the amount of biliary coloring matter; and in consistency, 
depending upon the amount of watery constituents and the increased 
peristalsis hurrying on the fluid intestinal contents. Diarrhoea charac- 
terized by the evacuation of much fluid is spoken of as serous; that 
in which there is much fecal matter, as stercoral; that in which the 
stools contain undigested food, as lienteric; and the profuse serous 
discharges occurring in and adding to the exhaustion of the last stages 
of severe diseases, such as tuberculosis, etc., as colliquative diarrhoea. 
Mucus is always present in greater or less amount, and microscopicly 
one may detect mucus, desquamated epithelial cells, particles of food 
(muscle fibers, starch granules, etc.), crystals of calcium phosphate and 
oxalate, cholesterin, and different microorganisms. 

In most cases there is more or less abdominal distress, which often 
amounts to severe, sometimes colicky, pain, and is often marked just 
before a stool. There is often also some abdominal distention, tympanites, 
borborygmi, and tenderness, and in case the lower colon be involved, 
tenesmus. The appetite is lessened or lost, the tongue is coated, thirst 
may be marked, and rarely there is vomiting (severe cases). The urine 
is lessened, sometimes greatly lessened, and may contain a little albumin, 
and indican and ethereal sulphates in excess. There may be, though 
usually there is not, slight fever. 

In very severe cases (primary infective enteritis) the pain may be 



CHRONIC ENTERITIS 659 

marked, vomiting severe, and the stools many and copious (resembling 
cholera: cholera nostras, cholera morbus); cramp-like pains in the calf 
muscles is common; and collapse attended by heart failure, cold ex- 
tremities, somnolence, and delirium may supervene. Many of these 
are undoubtedly cases of ptomaine or other food poisoning. 

Diagnosis. — The diagnosis is usually easy, though several days' 
observation is sometimes necessary to exclude certain infectious dis- 
eases — typhoid fever, dysentery, etc. Especial involvement of the small 
intestine is suggested by less frequent stools, borborygmi, colicky pain 
about the umbilicus, greenish or yellowish stools rather intimately mixed 
with mucus and containing particles of undigested food (lienteric stools), 
and the fact that a stool is often induced by taking food. Involvement 
of the large bowel is suggested by pain along the course of the colon, 
tenesmus, frequent fluid, "soupy," grayish stools, containing large 
flakes of mucus. Duodenitis is suggested by the development of jaun- 
dice (from the extension of the catarrhal inflammation to the bile duct). 

Prognosis. — The prognosis in general is good, the ordinary cases 
resulting in a cure in from three to five days. The manifestations, 
however, sometimes become chronic. The prognosis is often very serious 
in the infective form, as well as in debilitated subjects (tuberculous, 
cardiac, hepatic, and nephritic lesions). Children and debilitated 
subjects often die. 

Treatment. — The prime indication in all cases is to rid the intestine 
of all irritating substances — whence an initial purgative is called for in 
almost all cases, even in many cases in which the evacuations have been 
numerous. Mild cases respond well to w^arm applications to the abdo- 
men, 1 ounce (30 c.c.) of castor oil with 20 minims (1.25 c.c.) of tincture 
of opium, or calomel in repeated small doses, and restriction of the diet 
(milk, whey, and toast) for several days. It is well to give in addition 
intestinal antiseptics and astringents, such as the bismuth, salol, and 
chalk mixture (page 148), or a lead and opium pill (page 149). 
Resorcin, creosote, beta-naphthol, bismuth, and similar preparations 
are also useful. Involvement of the large bowel is best treated by 
cleansing enemas (to which boric or salicylic acid may be added), fol- 
lowed by a starch enema with tincture of opium. Depression is to be 
treated by stimulants, hot tea with whiskey or cognac, camphor, etc. 
The extreme depression that sometimes attends many serous evacua- 
tions, as well as the evacuations themselves, are often promptly con- 
trolled by morphine, £ grain (0.015 gram). Tonics are indicated during 
convalescence, and the diet must be regulated. 



CHRONIC ENTERITIS. 

Etiology. — Chronic enteritis is due to: (1) The repeated or long- 
continued action of the factors causing acute enteritis; (2) protozoan 
infection (amoeba trichomonas, cercomonas, balantidium, etc.) ; and (3) 



660 DISEASES OF THE INTESTINE 

it may occur secondarily to diseases of the heart, lungs, stomach, liver, 
and kidneys. 

Pathology. — The lesions are similar to those found in chronic gastritis, 
and are most frequent and marked in the lower part of the ileum and 
the colon. They consist of: (1) Hypertrophic processes — thickening 
of the mucosa (with the formation of much mucus), sometimes going 
on to polypoid masses, swelling of the solitary lymph nodes and plaques, 
follicular ulceration; and (2) atrophy — of the glandular tissue, with 
cicatrization, and consequent thickening of the intestinal wall. These 
two processes are often observed side by side. The follicular ulcera- 
tion sometimes leads to phlegmonous infiltration of the intestinal wall 
(in consequence of secondary infection); and in consequence of healing 
and cicatrization, stenosis sometimes results. 

Symptoms. — Several groups of cases may be distinguished: (a) In a 
minority of the cases the symptoms are much like those of the acute 
catarrh, although more mild. The patient has several diarrhceic- stools 
daily, attended by colicky pains and borborygmi, and in the event of 
involvement of the large intestine (as is usual) with tenesmus. The 
diarrhoea is extremely obstinate, especially in the event of ulceration, 
though even without it. In consequence of the common ulceration, blood 
and pus, and even particles of the necrotic tissue, may be found in the 
stools. (6) More common than diarrhoea is constipation, the consequence 
of atony of the intestinal musculature and comparative insensibility of the 
nerves of the mucosa, (c) In perhaps the majority of cases, periods of 
diarrhoea alternate with periods of constipation. During the period of 
constipation a thick mucus is secreted, feces accumulate, fermentative 
processes go on, the intestine becomes distended, and these culminate in 
such irritative processes as to result in rather marked serous evacuations. 
In some cases considerable mucus is secreted, and, becoming coagulated, 
forms masses or veritable casts of the intestines. In most cases well- 
marked nervous symptoms develop — apathy, headache, palpitation of 
the heart, somnolence, hypochondriasis, etc. Cutaneous manifestations 
(urticaria, pruritus), as well as tetany, attributable to auto-intoxication, 
are rarely observed. The patient frequently emaciates considerably, 
and a high grade of secondary anemia may develop. 

Diagnosis. — It is desirable to exclude specific ulceration — tubercu- 
lous, syphilitic, dysenteric, carcinomatous; as well as certain neuroses. 

Prognosis. — The prognosis is doubtful in many cases. In children and 
in the aged it is very bad. 

Treatment. — The treatment in general is similar to that of acute 
enteritis, but the strictest attention must be paid to dietetic and hygienic 
measures. In cases marked by alternate diarrhoea and constipation, 
special effort must be made to cure the constipation, since this is always 
an irritating factor. A clue to the correct diet may often be obtained 
by a study of the stools after the use of the Schmidt test diet (page 
652). In some cases no improvement follows until the patient is put 
upon the strictest dietetic regimen, whence the good results often attained 



DIARRHEAL DISORDERS OF CHILDREN 661 

at different spas and health resorts. The chronic lesions of the diseased 
mucosa are very resistant to medicinal measures, but certain good results 
seem sometimes to follow the administration of silver nitrate, lead acetate, 
zinc sulphate, bismuth preparations, naphthalene, tannic acid and drugs 
containing tannic acid. In involvement of the large bowel irrigation is 
useful, good results attending the use of sodium chloride solution, 0.6 per 
cent. ; silver nitrate, 0.02 to 0.05 per cent. ; boric acid, 0.5 per cent. ; sali- 
cylic acid, 0.1 per cent.; tannin, 0.2 to 0.5 per cent. 



DIARRHGSAL DISORDERS OF CHILDREN. 

(Summer Diarrhoea of Children; Gastro-enteritis of Children; Acute Gastro-intestinal 

Catarrh; Acute Dyspeptic Diarrhoea; Gastro-intestinal Intoxication; Cholera 

Infantum; Enterocolitis ; Ileocolitis; Infantile Dysentery.) 

Etiology. — Diarrhceal disorders are exceedingly common during the 
summer months (June, July, and August, but also May and September) 
among children, from the sixth to the eighteenth month. While espe- 
cially common among children of the poor, occurring frequently in tene- 
ment houses and asylums, they attack also those reared under the most 
favorable auspices. The special etiological factors are associated with 
diet, atmospheric temperature (summer heat), bad hygiene, and general 
inattention. Predisposing factors comprise feeble constitution, malnu- 
trition, marasmus, rickets, etc. According to Holt, only 3 per cent, of 
the fatal cases occur among breast-fed infants. 

The mild cases, so-called, acute dyspeptic diarrhoea, result from over 
feeding, too frequent feeding, the use of improper food, and the sudden 
change of food (such as may occur in weaning), and they are predisposed 
to by the heat and humidity of summer, fatigue, acute infections, etc. 
The feces usually contain the normal intestinal bacterial flora, no abnormal 
types being found with sufficient frequency to be considered of etiological 
significance. More severe cases, designated gastro-enteritis, gastro-intes- 
tinal intoxication, or cholera infantum, also result from the aforementioned 
causes; some of them are examples of acute milk poisoning, the bacteria, 
perhaps, having been destroyed by heat, but their toxins or ptomaines per- 
sisting; others are due to Bacillus dysenterise (Shiga) or allied organisms, 
Bacillus acidi lactici, Bacillus coli, Bacillus proteus, streptococci, staphy- 
lococci, etc., all of which, gaining access to milk, find therein conditions 
suitable for their growth. No one bacterial type is answerable for all 
cases, but any milk that contains a large number of any of these organ- 
isms may provoke the disorder. The type of disorder known as acute 
enterocolitis (ileocolitis) may result also from the aforementioned causes, 
but seems to be due in most cases to Bacillus dysenterise, although other 
organisms, such as the streptococcus, may participate in some of the 
lesions. This type of affection may occur as a primary disorder, or it may 
follow acute dyspeptic diarrhoea or gastro-enteritis (cholera infantum); 
it occurs as a terminal infection in measles, pneumonia, marasmus, etc., 



662 DISEASES OF THE INTESTINE 

especially in institutions. Bacillus dysenteriae is found especially in 
cases associated with mucus and blood in the stools, and its number is 
said to be proportionate to the severity of the infection. It is least 
common in purely fecal discharges, but may be isolated from the intes- 
tinal mucosa in fatal cases. Streptococci are often associated with 
Bacillus dysenterise. The mode of infection is not known, although it is 
attributed to the milk and water. There is some evidence of the con- 
tagious nature of some cases. The blood serum may give a positive 
agglutination test with Bacillus dysenterise. 

Pathology. — The lesions vary considerably in different cases, but 
they are usually confined to the colon and the lowermost parts of the 
ileum. In mild cases there is catarrhal inflammation of the small and the 
large intestine, with some swelling of the lymphoid follicles; in some 
cases the swelling of the lymphoid follicles forms a conspicuous feature. 
Many cases show necrosis and ulceration of the mucosa, sometimes 
limited to the follicles, sometimes more widespread. In severe cases 
pseudomembranous inflammation, usually limited to the mucosa, occurs, 
sometimes irregularly distributed, sometimes widespread — and is asso- 
ciated with submucous oedema and cellular infiltration. The diversity 
of the pathological lesions found associated with Bacillus dysenteriae, as 
well as the large number of associated bacteria, renders it impossible to 
differentiate the lesions due to the Shiga bacillus from those due to the 
other intestinal bacteria. In some cases a hyperplastic, followed by an 
atrophic, condition of the intestinal mucosa ensues and leads to general 
malnutrition. The mesenteric lymph nodes are swollen, the kidneys 
are the seat of cloudy swelling, and hypostatic congestion of the lungs and 
bronchopneumonia occur frequently. 

Symptoms. — Of the diarrhoeas of children, three types may be distin- 
guished: (1) Acute dyspeptic diarrhoea; (2) gastro-enteritis, gastro- 
intestinal intoxication, or cholera infantum; and (3) acute enterocolitis. 

Acute dyspeptic diarrhoea may commence insidiously or acutely, and 
may be seen in children of all ages. The attacks may be connected 
directly with the taking of deleterious food. In many cases, at first, 
aside from general restlessness and a little looseness and increased 
frequency of the bowels, the child presents no symptoms. After a day 
or two the stools increase in frequency, become very malodorous, and 
contain milk curds and other undigested food (if such has been taken). 
In other cases the onset is sudden, sometimes with convulsions, but 
usually with high fever (103° to 104° R), vomiting, diarrhoea, abdominal 
pain, tenderness, and distention. The stools vary much in number, and 
consist of malodorous yellowish or greenish-yellow feces, containing much 
gas, milk curds, and undigested food. Generally the attack subsides 
within three or four days (after the intestine has been relieved of irri- 
tating contents), but relapses are common, and the lesions may go on 
to a severe enterocolitis. 

Gastro-enteritis, g astro-intestinal intoxication, or cholera infantum 
is an extremely severe though uncommon intoxication (2 to 3 per 



DIARRHEAL DISORDERS OF CHILDREN 663 

cent, of the cases of summer diarrhoea, Holt), that usually develops 
suddenly in artificially fed children who have been subject to intes- 
tinal dyspepsia and diarrhoea. The disease is marked by sudden 
onset, high fever (105° to 106° F.), protracted vomiting, frequent serous 
intestinal discharges, marked prostration, frequent small pulse (130 to 
180 per minute), early collapse, and frequently early death. If there 
has been no preceding dyspeptic diarrhoea, the stools are at first copious 
and frequent, fecal in character, brownish or yellowish in color, and 
malodorous; soon they become greenish and later grayish, serous, watery, 
alkaline, and almost devoid of odor, or musty. There may be as many 
as twenty or thirty stools in the twenty-four hours. The vomiting is 
often uncontrollable and is augmented by food and drink. At first it 
consists of the contents of the stomach, highly acid or dense curds; 
later it becomes watery, mucoid, bile-stained, and less acid or alkaline. 
The general evidences of intoxication are marked from the beginning: 
prostration is extreme, the skin is ashen, the features pinched, the eyes 
and fontanelle sunken, the muscles flabby, the pulse rapid and feeble, 
the breathing shallow and rapid, the sensorium, at first excited, later 
becomes benumbed and the child listless; thirst is marked, the urine 
lessened, the tongue, at first coated and moist, becomes red and dry, 
and the abdomen retracted. Death may ensue within twenty-four 
hours in collapse with cold extremities though frequently high internal 
temperature. With the apathy and coma that precede dissolution, the 
vomiting and diarrhoea may cease (but should not be incorrectly inter- 
preted). In other cases the severe symptoms abate temporarily or 
permanently. The patient may remain for several days apathetic, 
semi-comatose; now and then there may be a convulsive seizure, the 
head may be retracted, and the respirations irregular, sometimes of the 
Cheyne-Stokes type (hydrencephaloid, or spurious hydrocephalus), 
Death may result at the end of three or four days; or the child may go 
into a speedy, though usually slow, convalescence — a marantic condi- 
tion (sclerema) persisting for some time; or convalescence may progress 
slowly or imperfectly and the child ultimately die of marasmus with 
irregularly recurring attacks of diarrhoea. 

Enterocolitis (ileocolitis, follicular enteritis, follicular dysentery), is 
the form of summer diarrhoea of children commonly associated with 
Bacillus dysenteriae, and characterized by necrotic and ulcerative 
processes in the ileum and the colon. It may follow acute dyspeptic 
diarrhoea, or any of the acute infectious diseases. The onset is 
usually gradual, though it may be abrupt. The fever increases 
and usually remains high (though hyperpyrexia is not as common 
as in cholera infantum). The stools become very frequent (12 to 30 
in twenty-four hours), small in amount, acid in reaction, malodorous, 
and contain mucus and streaks of blood. Though vomiting may 
occur, especially at the onset, it is rarely a conspicuous feature of the 
disease. The abdomen is distended and tender along the course of the 
ileum. Colicky pains may precede the stools, or the stools may be passed 



664 DISEASES OF THE INTESTINE 

painlessly, or there may be tenesmus if the lower colon and rectum are 
involved. In most cases the diarrhoea gradually subsides, the mucus 
and blood become less, the fever lessens, and the child may be convales- 
cent in two or three weeks. In other cases the convalescence is pro- 
tracted, the diarrhoea lessens but does not altogether disappear, and the 
general nutrition of the child suffers, though health may eventually 
be restored. 

In some cases the onset is abrupt and resembles dysentery in the 
adult. It is more common in elder children (past the third year), and 
begins with high fever, vomiting, severe abdominal pains, colonic 
tenderness, marked diarrhoea (frequent small stools containing much 
mucus and blood), tenesmus, marked intoxication, and great prostra- 
tion. Death may occur within forty-eight hours. Generally, however, 
the symptoms abate after twenty-four or thirty-six hours, but the child 
may continue ill for a week and finally succumb or go into a tedious 
convalescence. 

Under the designation coeliac disease has been described, especially 
by Gee, a variety of intestinal catarrh, of unknown cause, occurring in 
children from one to five years of age, and characterized by copious, 
diarrhceic, often frothy, and extremely malodorous stools, resembling 
oatmeal gruel (diarrhoea alba sive chylosa). The disease begins in- 
sidiously, and progresses frequently to a fatal termination, the con- 
spicuous general symptoms being asthenia, anemia, and emaciation. 

Diagnosis. — Acute dyspeptic diarrhoea is readily recognized by the 
fecal character of the stools, which contain undigested food and milk 
curds. It is well not to attribute any case to teething and similar 
factors, but to treat it as a disease from the beginning. Cholera infantum 
is distinguished by the high fever, incessant vomiting, serous discharges, 
general collapse, and other evidences of severe intoxication. The 
presence of mucus and blood in the discharges distinguishes entero- 
colitis. 

Prognosis. — The diarrhoeas of children are always serious, and the 
prognosis depends upon the previous condition of the child and the 
severity of the infection. Acute dyspeptic diarrhoea in a healthy child 
usually responds to treatment, but may prove fatal in a debilitated 
child. High fever, incessant vomiting, and extreme prostration are 
serious signs in cholera infantum. 

Treatment. — An essential part of the treatment is prophylaxis. Since 
most of the cases are related etiologically to the diet, that is, artificial 
diet, it is important to see that the milk is pure and fresh, that the dairy 
whence the milk is derived meets all modern requirements, that the 
milk is kept cool in transit, delivered fresh, and placed again on ice 
in the household. Pasteurization of fresh milk may be resorted to in 
hot weather as an additional measure of safety, and all bottles should 
be sterilized before being used. Additional safeguards consist in reduc- 
ing somewhat the diet (but not pure water) during the summer, and 
treating even the slightest symptom of intestinal disorder by stopping 



DIARRHEAL DISORDERS OF CHILDREN 665 

all milk for a day at least, and immediately cleansing the bowel by 
castor oil or small doses of calomel fa to -fa grain (0.003 to 0.006 
gram) three or four times a day. 

Hygienic Treatment. — Hygienic treatment is of the utmost impor- 
tance, and scarcely anything conduces so much to the comfort and health 
and recovery of the child as removal from the oppressive air of an over- 
crowded city to the cooler and more wholesome breezes of the country, 
mountains, or seaside. When this is impossible, the city child should be 
kept out of doors in the parks or on the river, and lightly clad. Frequent 
bathing (tepid water) is an excellent measure, and should be resorted 
to, especially if the temperature goes above 102° F. 

Dietetic Treatment. — The dietetic treatment is of paramount im- 
portance. At the onset of the attack of summer diarrhoea, milk must 
be absolutely prohibited. During the first twelve to twenty-four hours 
no food should be given, but pure water should be administered in 
amount equal to that of the fluid food to which the child has been ac- 
customed. In very young and marantic infants (under four months) 
it may be necessary to resort to food at the end of the first day, as the 
lesser of two evils, and pasteurized whey or barley water may be given in 
small amounts. In ordinary cases, however, it is advisable to discon- 
tinue milk for at least four or five days, and to substitute barley water 
(one tablespoonful of barley and a little salt to a pint of water and boil for 
half an hour, add hot water to make up for loss by evaporation, and 
strain); or rice water; or albumen- water (the whites of two or three eggs, 
1 pint of water, 1 dram of brandy, and a little salt) ; or beef juice. Older 
children (three or four years) may be permitted chicken broth, mutton 
broth, or beef broth, but caution in the use of broths is necessary, since 
of themselves they are laxative. In some cases the intolerant stomach 
may be made more retentive by lavage with warm saline solution, and 
in the event of insufficient water being introduced by the mouth, recourse 
may be had to enteroclysis. The return to milk diet must be gradual, 
small amounts of a suitable mixture, well diluted, being added day by 
day, and being discontinued upon the slightest return of intestinal de- 
rangement. In the majority of cases satisfactory milk mixtures may be 
readily prepared by diluting whole milk one-fourth, one-half, or three- 
fourths with sterile water or barley water and adding 5 per cent, of lime 
water and a sufficiency of milk sugar to bring the mixture to the desired 
percentage. Ordinary whole milk contains : fat, 4 per cent. ; sugar, 4.5 per 
cent. ; and proteins, 3.5 per cent. Twenty ounces is a convenient amount 
of the mixture to make at one time. By adding 5 ounces of whole milk to 
1 ounce of lime water, 1 ounce of milk sugar, and enough water to make 20 
ounces, a mixture is obtained that approximates: fat, 1 per cent.; sugar, 
6 per cent.; and proteins, 0.9 per cent. Ten ounces of milk and the 
other ingredients, as mentioned, make a mixture approximating: fat, 2 
per cent.; sugar, 7 per cent.; and proteins, 1.8 per cent. Fifteen ounces 
of milk, the lime water and water as mentioned, and J ounce of milk 
sugar make a mixture approximating: fat, 3 per cent. ; sugar, 5.5 per cent. 



666 DISEASES OF THE INTESTINE 

and proteins, 2.7 per cent. In most cases one or the other of these mix- 
tures usually suffices. One should begin with the weaker and proceed 
to the stronger, remembering that the infants usually can digest fats 
more easily than proteins. In intractable cases resort should be had to 
more accurately prepared mixtures. Whey and cream mixtures rather 
than milk may be found advantageous in many cases for a time at least. 
A wet-nurse is sometimes advisable. 

Medicinal Treatment. — Medicinal treatment is in many cases 
subsidiary to the foregoing. Since, however, all cases are due to infec- 
tion of the intestinal contents, and later to infection of the intestine 
itself, the bowel should be immediately cleared by castor oil, or small 
and repeated doses of calomel (especially useful in the event of vomiting), 
or by lavage and colonic irrigation. In acute dyspeptic diarrhoea these 
measures with regulation of the diet often suffice, though bismuth sub- 
nitrate (or subcarbonate, subgallate, salicylate, or beta-naphthol), is 
useful for its restraining influence on the bowel. In very severe cases, 
bismuth, salol (or resorcin), and chalk mixture will be found useful; if 
diarrhoea persists, a little deodorized tincture of opium may be added, 
but it should not be given until the intestinal tract has been thoroughly 
cleansed. Pain until then may be relieved by a spice poultice, or spirit 
of chloroform or camphor. 

In cholera infantum, which may be serious and even alarming from 
the outset, the stomach and intestines should be cleansed with saline 
solution, or in the event of very high fever, ice water may be used by 
the bowel, or the child put in a tepid bath, and the water gradually 
reduced by the addition of ice. An ice-bag should be applied to the 
head. Morphine, t ^q- grain (0.0006 gram), and atropine, -g-J-g- grain 
(0.00008 gram), to a child one year old, may be given hypodermicly 
to allay irritation, and to overcome the effects of the toxemia on the 
nervous system. It is especially valuable if the vomiting and purging 
persist and the child collapses. The dose may be repeated in an hour 
if no improvement has resulted. To replace the lost body fluids, as 
well as to reduce the toxemia, enteroclysis or hypodermoclysis is of 
great service. Small amounts, 20 to 40 c.c, repeated, are sometimes 
more serviceable than a single large dose (250 c.c). In the collapse of 
some cases small amounts of caffeine (1 to 400), or of adrenalin chloride, 
added to the saline solution, may prove useful. Stimulants are indicated 
in severe cases; sometimes small amounts of brandy, cognac, or cham- 
pagne may be retained when all else is rejected. Strychnine may be 
given hypodermicly. When the vomiting has been overcome, bismuth and 
the remedies previously mentioned, are sometimes efficacious, or starch 
water and laudanum may be given by the rectum. Return to feeding 
must be done gradually, beginning with albumin water and beef juice; 
later whey and cream, peptonized milk, or the milk mixtures men- 
tioned may be given. If convalescence is protracted and diarrhoea per- 
sists, or is easily provoked, the diet should be looked to ; but the condition 
may be one of enterocolitis, in which event injections of saline solution 



PHLEGMONOUS ENTERITIS 667 

or silver nitrate (1 to 10,000) may be serviceable. Iron, arsenic, cod-liver 
oil, and change of climate are of marked service during convalescence in 
many cases. An effective serum for Bacillus dysenterise infections 
has not yet been produced. 



CROUPOUS OR DIPHTHERITIC ENTERITIS. 

Croupous or diphtheritic enteritis is an inflammation of the intestinal 
mucosa attended by necrosis and the formation of a croupous (or 
fibrinous) exudate. 

Etiology. — Croupous or diphtheritic enteritis is due to: (1) Bacterial 
infection — whence it occurs in certain infectious diseases, such as 
pneumonia (the pneumococcus may be isolated from the exudate in 
some cases), typhoid fever, scarlet fever, smallpox, and septic processes. 
(2) It occurs in conditions of reduced vitality, such as occur in chronic 
diseases, when it is frequently a terminal infection, as in nephritis, 
cirrhosis of the liver, heart disease, carcinoma, etc. — the reduced vitality 
permitting of secondary bacterial infection. (3) It occurs also in poison- 
ing by mercury, arsenic, ammonia, lead, etc. 

Pathology. — The lesions vary in different cases. In the one there is 
necrosis of the mucous membrane, varying in extent and depth, but often 
confined to the tops of the folds of mucous membrane and rather super- 
ficial. In other cases the necrosis is more widespread and may involve 
the entire thickness of the mucosa. The false membrane is grayish, 
grayish yellow, or grayish white in color, and is surmounted on a congested 
base. The lesions are more common in the colon than in the small 
intestine. In the second group of cases the solitary lymph nodes are the 
seat of swelling and superficial or deep necrosis, attended by the formation 
of a membranous exudate. 

Symptoms. — Often there are no symptoms. When present, the symp- 
toms are those of enteritis and colitis. The exact nature of the disorder 
cannot be recognized unless some of the exudate is discharged with the 
stools. 

Treatment. — The treatment is that of the primary affection plus that 
of catarrhal enteritis. 



PHLEGMONOUS ENTERITIS. 

Phlegmonous enteritis is a rare disease characterized by suppurative 
inflammation of the mucous and muscular coats of the intestine. As an 
idiopathic affection it is exceedingly rare (even rarer than phlegmonous 
gastritis) ; as a secondary affection it sometimes attends pyococcic pro- 
cesses, and may be associated with intestinal intussusception or strangu- 
lation or strangulated hernia. Anatomically the purulent collection may 
be circumscribed (abscess) or diffuse (phlegmon). The symptoms are 



668 DISEASES OF THE INTESTINE 

usually those of peritonitis, and the affection is scarcely susceptible of 
differential diagnosis. The treatment, apart from operative procedures 
in association with intestinal obstruction, is unavailing. 



APPENDICITIS. 

Etiology. — Inflammation of the vermiform appendix is an extraordin- 
arily common disorder : the commonest intra-abdominal disease. It is most 
common in early adult life, and more common in men than in women. It 
is really the consequence of infection occurring in an organ provided with 
a precarious blood supply and ill adapted to drainage — both of which 
in circumstances permit of the ready operation of bacteria. The factors 
impeding drainage are the excessive length of the organ, the narrowness 
and often tortuosity of the lumen, Gerlach's valve, and the swelling 
of the mucosa that readily occurs. To these one may, perhaps, add the 
influence of appendicular calculi — which are not fecal concretions in a 
true sense, but the result of appendicular inflammation; when formed, 
they tend to keep up the inflammation, and by pressure, attrition, and 
interfering with local blood supply they are a factor in determining the 
site of ulceration. Foreign bodies and worms are rarely found in the 
appendix, but when occurring may be of etiological significance. The 
chief infectious cause is Bacillus coli, but streptococci, staphylococci, 
pneumococci, Bacillus influenzae, Bacillus typhosus, Bacillus dysenterise, 
Bacillus tuberculosis, Streptothrix actinomyces, and other organisms 
may be the active etiological agent. 

Pathology. — Acute and chronic cases may be distinguished. The 
lesions of the acute cases comprise the ordinary phenomena of inflam- 
mation, congestion, oedema, round-cell infiltration, etc., which very 
rarely may be limited to the mucosa (so-called catarrhal appendicitis). 
In most cases the lesions, although they vary much in many cases, 
extend more or less throughout the wall of the appendix. Sometimes 
they consist only of the aforementioned inflammatory phenomena, with 
perhaps only a little superficial erosion of the lining mucosa (acute 
interstitial appendicitis). But in the great majority of cases in which 
the lesions are widespread or severe there is more or less suppuration, 
necrosis, and loss of the mucosa (ulcerative appendicitis); the lesions 
may or may not progress to perforation of the organ. In other cases, in 
consequence of virulent infection or defective or abolished blood supply, 
gangrene supervenes. The chronic lesions also are rarely, perhaps, 
confined to the mucosa (chronic catarrhal appendicitis). In the great 
majority of cases, however, all the coats of the organ are involved, the 
conspicuous changes consisting of connective-tissue hyperplasia of the 
submucosa and the muscularis, round-cell infiltration, and atrophy of 
the muscular tissue. In some cases, the mucosa having been the seat 
of more or less suppuration and necrosis, is finally entirely lost, and 
the opposed ulcerating surfaces by a process of organization may become 



APPENDICITIS 669 

united into a firm fibrous union with obliteration of the lumen throughout 
more or less of the length of the organ (chronic obliterative appendicitis). 
Most of the chronic cases are subject to acute exacerbations — in which 
to the chronic hyperplastic process acute manifestations may super- 
vene (recurring or relapsing appendicitis). In many of these cases the 
appendicular contents become and remain purulent (chronic empyema) ; 
and at any time any of the severe acute lesions, such as perforation or 
gangrene, may supervene. 

The chief significance of appendicitis attaches to the peritonitis it 
provokes. In mild cases this may be strictly localized to the region 
about the appendix, and serous or serofibrinous in character. In many 
severe cases, usually with, but often without, perforation, the peritoneal 
lesions may also remain localized, but they become purulent in char- 
acter — so-called peri-appendicular abscess. Limiting adhesions may 
suffice to " wall-off " the abscess from the rest of the peritoneal cavity, 
but in many cases the pus finds its way into the pelvis, or by a progressive 
breaking down of adhesions and the formation of new adhesions in 
advance of the old ones, more or less of the peritoneal cavity may ulti- 
mately become involved (progressive fibrinopurulent peritonitis). In 
some cases there are few, if any, adhesions, the peritoneum constituting 
a veritable pus sac (diffuse or generalized suppurative peritonitis). Oc- 
casionally the lesions become putrid. Rarely the peritoneum is found 
quite dry and lustreless — in cases of very severe and overwhelming 
intoxication (toxic peritonitis). The peri-appendicular abscess is some- 
times situated behind the peritoneum, about the kidney, near the liver. 
These extraperitoneal as well as intraperitoneal collections of pus may 
burrow in various directions — into the intestine, into the pelvis (and 
be discharged through the rectum or vagina), behind the liver, through 
the diaphragm, and be expectorated through a bronchus, etc. Multiple 
abscesses of the liver (suppurative pylephlebitis) is a common complica- 
tion in neglected cases; general septicopyemia also may ensue. Pri- 
mary carcinoma is not uncommonly found in appendices removed for 
appendicitis. 

In chronic appendicitis, in addition to the lesions already mentioned, 
peritoneal adhesions are usually found. These, binding the appendix 
to adjacent organs, are, in large part, the cause of the symptoms of 
chronic appendicitis, and may lead to strangulation or kinking of the 
appendix or intestine and various disturbance of the organs to which 
they may be attached. 

Symptoms. — In acute appendicitis the onset is usually sudden. The 
chief symptoms consist of severe abdominal pain, nausea and vomiting, 
tenderness and muscular rigidity in the region of the appendix, and fever 
(101° to 103° F.). The pain is usually sudden in onset and severe, often 
colicky in character. It is usually at first epigastric or umbilical in situation, 
or may be diffuse; but it soon becomes localized to the right lower abdom- 
inal quadrant. It may radiate to the bladder, to the testicle, or the lumbar 
region; and may be aggravated by movement of the right thigh, which is 



670 DISEASES OF THE INTESTINE 

often flexed to relieve the pain. Tenderness also may be more or less 
general at first, but it soon becomes localized to the region of the appen- 
dix, and is usually most marked at McBurney's point (a point midway 
on a line drawn from the anterior superior spine of the ilium to the 
umbilicus). In some cases depending upon the direction of the appen- 
dix, the tenderness may be most marked in the lumbar region (retro- 
peritoneal appendix pointed upward), in the pelvis, to the left of the 
median line, etc. The rigidity of the muscles in the right lower abdom- 
inal quadrant may be very marked. At the onset, accompanying the 
fever, the pulse is usually rapid, and a polynuclear leukocytosis com- 
monly supervenes (12,000 to 25,000). The bowels are usually consti- 
pated, and painful; and perhaps frequent micturition may occur if the 
appendix reaches into the pelvis and impinges on the bladder. 

In the course of a day or two the lesions and the symptoms may sub- 
side and the patient may go on to apparent recovery. Seeming improve- 
ment, such as lessening of pain and of the fever, however, by no means 
indicates subsidence of the inflammatory phenomena; both the pain 
and fever may lessen in cases attended by perforation and suppuration. 
The pulse is a much better index of the intra-abdominal conditions 
than is the pain or the fever. In the cases that do subside the appendix, 
usually does not return to its previous normal condition, and recurrences 
and relapses are likely to ensue. 

In the cases that do not improve, more or less severe peritoneal 
lesions develop — either a peri-appendicular abscess or diffuse peri- 
tonitis. The peri-appendicular abscess may be recognized by a more 
or less well-defined mass in the region of the appendix; it is usually 
doughy to the touch and may disclose deep oedema; it is dull on percus- 
sion or perhaps tympanitic from overlying and distended intestinal 
coils; and on auscultation it reveals no peristaltic sounds. This abscess 
may follow directly upon what seemed to be a relatively mild appen- 
dicitis; that is, there may be no signs whatever suggesting a perforation 
or other serious complication. Occasionally sudden severe pain does 
occur, and may be interpreted as rupture of the appendix. Generalized 
peritonitis is disclosed by generalized pain, tenderness, and rigidity, 
vomiting, rapid feeble pulse, fever, leukocytosis, Hippocratic counte- 
nance, and other evidences of marked intoxication, and final collapse. 
This generalized peritonitis may be preceded by more or less well-defined 
evidences of localized abscess, or it may develop directly in consequence 
of rupture or gangrene of an appendix not enclosed within adhesions. 

Chronic appendicitis is characterized clinically by various gastro- 
intestinal and neurasthenic manifestations. The chief symptoms are 
comprised within the term indigestion (Moynihan's appendix dyspepsia); 
to which may be added frequent or infrequent attacks of more or less 
well-marked or frank appendicitis. The dyspeptic phenomena simu- 
late and are readily mistaken for disease of the gall-bladder, gastric 
ulcer (exaggerated activity of the pylorus, pylorospasm), etc., and often 
can scarcely be distinguished therefrom aside from operative inter- 



APPENDICITIS 671 

vention. Well-marked neurasthenia is quite common and the patient 
may emaciate. Mucous colitis also may be a manifestation of chronic 
appendicitis. 

Diagnosis. — Sudden severe abdominal pain, nausea and vomiting, 
tenderness and muscular rigidity in the region of the appendix, and 
fever, usually suffice for the diagnosis in the acute cases. However, 
in some cases one has to take into consideration the possibility of 
the many acute abdominal conditions that may cause sudden pain, 
nausea, and vomiting, especially perforated gastric or duodenal ulcer, 
gallstone colic, renal colic, intestinal colic, menstrual pains, acute 
pancreatitis, DiehPs crisis in floating kidney, intestinal intussusception 
and strangulation, etc.; but these and other abdominal disorders are 
in themselves well characterized symptomatically and scarcely any one 
of them is likely to present all the characteristic symptoms of acute 
appendicitis. Chronic appendicitis may be recognized in the cases that 
do not present unequivocal symptoms, in the cases in which dyspepsia 
is the obtrusive feature, by bearing in mind that most cases of intractable 
dyspepsia have an anatomical basis, and that this is usually gastric 
ulcer, gastric carcinoma, perigastric adhesions, chronic cholecystitis, with 
or without gallstones, chronic pancreatitis, or chronic appendicitis. 

Prognosis. — The prognosis in acute cases is extraordinarily uncertain, 
since no one can foretell in the early stage whether the disease is likely 
to be mild or severe; the symptoms bear no constant relationship to the 
severity of the lesions (the most grave anatomical lesions may be present 
with mild or slight symptoms); and apparent improvement may occur 
with advancing intra-abdominal conditions. In the event of recovery, 
relapses and recurrences are likely. The outlook in the chronic cases as to 
permanent relief is bad unless recourse is had to surgical intervention. 

Treatment. — The treatment of appendicitis is surgical; there is no 
really dependable effective medical treatment. It is true that some 
patients recover under medical treatment, and it is also true that many 
die who might be saved by timely resort to surgical measures. Fur- 
thermore, it is true that some patients die after an operation, but the 
great majority of these are subjects in whom the operation has been 
unduly delayed or they are the subjects of fulminating infections — doomed 
from the very outset. The mortality following a timely operation is 
much less than under any other form of treatment. The foregoing 
are the facts that should guide us in our treatment, and operation 
should not be delayed until the patient is "sick enough" to warrant it. 

Pending the arrival of the surgeon, and in any event as soon as the 
patient is seen, all food and water should be stopped (and none should 
be given until the patient is recovering); the stomach should be washed 
out, and the procedure repeated if nausea and vomiting continue; and 
the bowels should be opened by an enema. If the patient is seen early, 
before the development of peritonitis, the bowels may be unloaded by 
castor oil, but if peritonitis (local as well as general) has supervened, 
no cathartics should be given by the mouth. An ice bag may be applied 



672 DISEASES OF THE INTESTINE 

to the abdomen to relieve pain, or hot, moist compresses, if these are 
more grateful to the patient. Ochsner recommends hot boric-acid solu- 
tion and alcohol. Enteroclysis by the drop, or the Murphy, method may 
be used to relieve thirst; perhaps it has also some good effect on the 
developing peritonitis. If deemed necessary, stimulants and liquid 
meat extracts (which, however, contain more alcohol than nutriment) 
may be added to the physiological saline solution, and given three or 
four times a day. Opium should be entirely withheld if possible; it 
should never be given until the diagnosis is at least reasonably certain, 
and then only the smallest possible amount, sufficient only to mitigate 
the pain and not obtund the sensibilities and mask the symptoms. 



SIGMOID DIVERTICULITIS. 

(Perisigmoiditis.) 

Etiology. — Aside from congenital diverticula of the intestine, of which 
the most common is Meckel's diverticulum, acquired diverticula may 
occur almost anywhere in the intestine, sometimes in the region of the 
appendix, but most commonly in the sigmoid flexure of the colon. The 
cause of the condition is not well understood. They are common in 
elderly obese subjects who have been constipated. They have been 
attributed to localized areas of muscular weakness, and are often related 
to the absorption of the fat of epiploic appendages. 

Pathology. — In the sigmoid these diverticula occur either in two parallel 
rows along the sides of the intestine or along the attachment of the 
mesentery; they may be confined to the epiploic appendages. There 
may be several or many. They vary in size from 1 to 2 mm. in diameter 
to a centimeter or more. When small they are usually spheroidal; but 
when elongated they are likely to be flask-shaped. They commonly 
communicate with the lumen of the gut by a constricted orifice. They 
become the seat of more or less well-marked inflammation, which in 
acute cases may be catarrhal, suppurative, or gangrenous ; and this may 
give rise to localized peritonitis with abscess formation or to generalized 
peritonitis— in all of which respects the lesions are somewhat analogous 
to appendicitis. More or less inspissated fecal matter and even enter- 
oliths may be found within the pouches. In the chronic cases there is 
usually much connective-tissue hyperplasia and consequent thickening 
and stenosis of the bowel (chronic hyperplastic sigmoiditis and peri- 
sigmoiditis). The condition much resembles and has been mistaken for 
carcinoma. 

Symptoms. — The acute cases most simulate acute appendicitis, the 
pain, tenderness, and muscular rigidity, however, being on the left side. 
(As is well known, this may occur in appendicitis, when the appendix 
reaches over to the left side or depends into the pelvis.) The lesions 
may go on to abscess formation and divers suppurative complications. 
In the chronic cases the symptoms consist of constipation, gradually 



ULCERATION OF THE INTESTINE 673 

increasing colonic obstruction, and a tumor mass in the left inguinal 
region. These occurring in an elder person (usually a man), simulate 
carcinoma. Doubtless some supposed carcinomas of the sigmoid 
removed at operation were in reality cases of sigmoid diverticulitis. 
This sigmoiditis, rather than carcinoma, is suggested by long-standing 
constipation, gradually increasing intestinal obstruction, absence of blood 
in the feces, and slight anemia and cachexia. 

Prognosis. — The outlook is good under appropriate treatment. 

Treatment. — The treatment is wholly surgical and consists of removing 
the diseased portion of the sigmoid. 



ULCERATION OF THE INTESTINE. 

Etiology. — The following forms of ulceration of the intestine are de- 
scribed by Nothnagel : (1) Ulceration due to necrotic processes — simple 
duodenal ulcer, ulcer following burns, embqlic and thrombotic ulcers 
(including those seen in patients with multiple neuritis), and amyloid 
ulcers. (2) Ulceration due to inflammatory processes — catarrhal ulcer, 
follicular ulcer, and stercoral or decubital ulcer. (3) Ulceration due to 
acute infectious diseases — typhoid fever, dysentery, diphtheria, anthrax, 
sepsis, erysipelas, and varioloid. (4) Ulceration due to chronic infectious 
diseases — tuberculosis, syphilis, leprosy, and pellagra. (5) Ulceration due 
to constitutional disease — gout, scurvy, and leukemia. (6) Ulceration 
due to intoxications — uremic ulcer, mercurial ulcer. 

Symptoms. — Duodenal ulceration, as well as typhoid, dysenteric, and 
diphtheric ulceration, are discussed elsewhere. Diarrhoea with blood, pus, 
mucus, and shreds of necrotic tissue in the stools are the important 
symptoms of ulceration of the intestine. Although diarrhoea is common, 
it is not invariable and may be absent in the presence of even extensive 
ulceration. Nothnagel believes that the presence or absence of diarrhoea 
is determined primarily by the site of the ulcerative lesions, stating that 
if the ulcers are in the small intestine, cecum, or ascending colon they 
probably never produce diarrhoea unless the ulceration is complicated 
by other conditions, such as intestinal catarrh, amyloid disease, special 
forms of infection, or other factors that may influence directly intes- 
tinal peristalsis. If the ulcers are in the lower portion of the colon and the 
rectum, diarrhoea occurs with great regularity, but it may be absent 
if the ulcers are few in number and if the nervous irritability of these 
portions of the bowel is lowered or inhibited. Blood is often present, 
but it may be absent, and if present may be due to causes other than 
ulceration. It is a valuable sign when it occurs in circumstances that 
render likely the presence of ulceration. Pus is usually present in greater 
or less amount, and often requires careful search to detect it; it is of 
greater diagnostic significance than the presence of blood. Large 
amounts indicate perforation into the intestine of an extra-intestinal 
abscess (periappendicular, peri-uterine, etc.), the presence of a suppurat- 
43 



674 DISEASES OF THE INTESTINE 

ing and ulcerating carcinoma, or a croupous inflammation of the intestine. 
A purulent mucus is sometimes present, and in some cases one may 
encounter peculiar sago-like grains of mucus, formerly but no longer 
considered diagnostic of follicular ulceration. Shreds of tissue (mucosa, 
connective tissue, and even muscularis) are important diagnostically, 
but they are rather rare. Pain may or may not be present; it is of value 
only when present continuously at the one place and intensified by press- 
ure. If the ulceration is slight the general nutrition is not much impaired, 
but extensive ulceration usually leads to marked deterioration of the 
general health. Secondary infection of the ulcer may cause a little fever, 
but usually there is none. Perforation is not uncommon, and may give 
rise to local or generalized peritonitis, or to a retroperitoneal abscess. 

Diagnosis. — The diagnosis of the nature of the ulceration may some- 
times be made by attention to the attending phenomena and examina- 
tion of the stools for tubercle bacilli and other specific organisms, as well 
as shreds of tissue. Tubercle bacilli in the stools, however, may have 
been swallowed, and do not necessarily mean ulceration of the intestine. 

Prognosis. — The prognosis varies with the nature of the etiological 
factors. 

Treatment. — The treatment in many cases is determined by the nature 
of the primary disorder; the treatment of the primary and the secondary 
conditions is not separable — such as ulcers occurring in infectious dis- 
eases (typhoid fever, dysentery, tuberculosis, syphilis, etc.), in constitu- 
tional diseases, in poisoning, etc. In all cases regulation of the diet is 
of the utmost importance, a suitable diet being determined upon largely 
by a study of the individual patient. Direct treatment of the ulcers, by 
means of topical applications or rectal enemas, is scarcely possible unless 
the ulcers are situated in the rectum or the lower part of the colon, 
though in some cases even the ascending colon may be reached by 
enemas. The most suitable medicated enemas consist of boric acid or 
salicylic acid (0.3 to 0.5 per cent.), thymol (0.1 per cent.), silver nitrate 
(0.3 to 1 per cent.), or tannic acid (0.3 to 1 per cent.). Recently some 
good results have been achieved by the operative establishing of an arti- 
ficial anus through the medium of the cecum and the giving of complete 
rest to the colon; in other cases, a communication has been established 
with the exterior through the medium of the cecum or the appendix and 
the entire colon and the rectum subsequently periodically irrigated with 
medicated enemas, with asserted good results. Internally few prepara- 
tions are of much service; but some relief may be afforded the patient 
by the symptomatic treatment of diarrhoea, pain, hemorrhage, etc. 



INTESTINAL OBSTRUCTION. 

The term intestinal obstruction is inclusive; it comprises a number of 
somewhat different though related conditions, to which several names 
have been applied : Occlusion signifies a complete closure of the lumen 



INTESTINAL OBSTRUCTION 675 

of the intestine entirely arresting the onward passage of the intestinal 
contents. Stenosis signifies a lessening of the lumen of the intestine, 
an incomplete occlusion, arising from any cause whatsoever — a con- 
dition in which the onward passage of the intestinal contents is 
impeded, but not arrested. Stricture signifies a lessening of the lumen, 
the result of disease (usually annular) of the wall of the intestine. 
Constriction signifies lessening of the lumen of the intestine in con- 
sequence of pressure (compression) or traction from without. Obtura- 
tion signifies obstruction from within the lumen of the intestine, as by 
impacted feces, an enterolith, a gallstone, etc. Incarceration signifies 
an imprisonment of the intestine in a part or cavity. Strangulation 
signifies a form of constriction in which the compression is so severe 
as to interfere seriously with the vascular and nervous supply, and 
hence the functional activity and even the life of the intestine. The 
term ileus is sometimes inappropriately applied to any severe intes- 
tinal obstruction or occlusion attended by stercoraceous vomiting; 
and the term paralytic ileus is sometimes applied to the paresis or 
paralysis which may follow abdominal operations, the relief of intes- 
tinal obstruction (release from constricting bands, rectification of a 
volvulus, etc.), or that occurs in peritonitis, etc., and sometimes even 
without anatomical basis. 

Etiology. — Intestinal obstruction may be due to : 

1. Disease Outside the Intestine: (a) Tumors of any of the intra- 
abdominal organs, especially of the ovary, uterus, omentum, or kidney, 
which give rise to obstruction by compression, the obstruction being 
usually chronic, though the symptoms may develop acutely. Analogous 
in action to tumors are abscesses, especially pelvic and peri-appendicular, 
as well as collections of fluid, such as pancreatic cysts and hydronephrosis. 
(6) Conditions causing strangulation, such as internal hernia (diaphrag- 
matic, subcecal, duodenojejunal, intersigmoid, through the foramen of 
Winslow); post-inflammatory adhesions and bands, pedicles of tumors, 
remains of fecal structures, such as Meckel's diverticulum (especially 
when adherent at its unattached end), fibrous remains of fcetal vessels, 
etc., beneath which a loop of intestine may slip and become constricted, 
or which by traction may occasion kinking of the intestine; omental and 
mesenteric slits and peritoneal pouches, which may engage and strangle a 
portion of the bowel; etc. Strangulation is the most common cause of 
acute intestinal obstruction (34 per cent, of the cases, Fitz). Seventy 
per cent, of the cases occur in men; 40 per cent, between the fifteenth and 
thirtieth years. In 90 per cent, the small intestine is involved; in 87 
per cent, the strangulation is in the right iliac fossa; and in 83 per 
cent, in the lower half of the abdomen (Fitz). 

2. Disease of the Intestinal Wall: (a) Intussusception or invagina- 
tion, the infolding of the intestine into itself, is a common cause of 
acute obstruction (31 per cent, of the cases, Fitz), and occasionally causes 
chronic obstruction. It is twice as common in males as in females ; more 
than one-half of the cases occur before the tenth year, and many occur in 



676 DISEASES OF THE INTESTINE 

the first year of life when the intestine is relatively long and irregular; 
peristalsis (an essential cause of the disorder) is very common. The 
invagination is always a descending process, the upper portion of the 
bowel descending into the lower — whence several varieties are recognized : 
the iliac, in which the ileum alone is involved; the ileocecal, in which 
the ileocecal valve enters the colon (75 per cent, of the cases) ; the ileocolic, 
in which the lower part of the ileum passes through the ileocecal valve; 
the appendiceal, in which the vermiform appendix enters the cecum; 
the colic, in which the colon alone is involved; and the colicorectal, in 
which the colon descends into the rectum. The intussusception forms 
an irregular tumor varying from less than an inch to a foot or two in 
length. It consists of three layers — an outermost or receiving layer, a 
middle or returning layer, and an innermost or entering layer. The 
intussuscepted intestine is usually red, congested, and much swollen, and 
about it there is more or less peritonitis. The compression of the mesen- 
teric vessels, especially those supplying the middle and the innermost 
layers, is often so extreme as to lead to rupture and hemorrhage from 
the mucous lining and consequent blood in the stools — an important 
diagnostic feature. Sloughing of the invaginated portion of intestine 
sometimes results, and should the middle and the outermost layers 
have become adherent, spontaneous cure may ensue — of which some 
remarkable instances, with the discharge by the rectum of large portions 
of the bowel, have been recorded. 

(b) Volvulus or twist is a fairly common cause of acute intestinal 
obstruction (about 15 per cent, of the cases). It occurs twice as commonly 
in males as in females, is most frequent in the fourth decade of life, 
involves the sigmoid flexure in 50 per cent, of the cases (less commonly 
the cecum and the small intestine) ; and is usually axial and associated 
with a long, non-fatty mesentery. The twist seems sometimes to have 
been provoked by a trauma or severe diarrhoea. 

(c) Tumors of the intestine are a rather common cause of chronic 
obstruction. Cylindrical epithelioma (carcinoma) is the most common. 
It is usually annular (rarely circumscribed), involves most commonly 
the sigmoid flexure or the descending colon, and gives rise to a gradual 
lessening of the lumen of the bowel, until in some cases occlusion is almost 
if not quite complete. It is more common in males than in females, and 
occurs especially beyond the middle period of life (except carcinoma of 
the rectum, which is remarkably common in early adult life). Sarcoma 
is much less common than carcinoma. Benign growths, such as polyps, 
adenomas, and fibromas, have been reported. 

(d) Cicatricial strictures sometimes cause chronic obstruction. The 
lesions are most common in the large intestine, and follow the healing of 
dysenteric ulcers (colon), syphilitic ulcers (rectum), follicular ulcers, 
tuberculous ulcers, and rarely typhoid ulcers. Occasionally the stricture 
is congenital. 

(e) Peritonitis, occasioning paralytic distention, is not an uncommon 
cause of acute or subacute intestinal obstruction. 



INTESTINAL OBSTRUCTION 677 

3. Abnormal Intestinal Contents: (a) Fecal impaction (coprostasis) 
is a rather common cause of chronic intestinal obstruction, though the 
symptoms may develop acutely. The accumulation usually occurs in the 
cecum or the sigmoid flexure. It may occur at any age, but is most 
common in children, adult women, and in aged, debilitated, hysterical, 
hypochondriacal, and insane subjects. The accumulation is sometimes 
enormous, and may be favored by congenital dilatation of the colon, 
though habitual inattention to the bowels also may result in atony, 
distention, and excessive accumulation. The retained fecal masses 
become very hard, but often permit the passage by them of fluid feces 
(sometimes interpreted as evidence of the absence of accumulation). 
Occasionally inflammation and ulceration of the bowel results, (b) 
Gallstones having ulcerated through the gall-bladder into the small 
intestine sometimes cause obstruction, usually at the ileocecal region, 
but sometimes in the duodenum. Obstruction is rare if they ulcerate 
into the colon, (c) Enteroliths formed by the deposition of magnesium 
and calcium salts, especially phosphates, about divers nuclei, such as 
hard feces, a small gallstone, hair, etc., may cause obstruction, (d) 
Foreign bodies, such as fruit seeds, buttons, coins, etc., as well as large 
collections of tangled round worms, and occasionally large amounts of 
bismuth or magnesium taken medicinally, have been known to cause 
obstruction. 

Pathology. — The anatomical results of acute obstruction consist of 
dilatation of the intestine above the obstruction together with the accu- 
mulation of feces and gas, and narrowing of the lumen or collapse of 
the intestine below the obstruction. In chronic obstruction, above the 
obstruction there is more or less dilatation of the intestine and hyper- 
trophy of its walls, the latter developing in consequence of the long- 
standing difficulty to the onward movement of the feces. The intestinal 
wall, especially the mucous membrane, is often inflamed and ulcerated, 
and perforation or spontaneous rupture and consequent peritonitis are not 
unknown. 

Symptoms. — Clinically intestinal obstruction may be acute or chronic. 
Acute obstruction results from strangulation, intussusception, volvulus, 
foreign bodies, and peritonitis; chronic obstruction results from tumors, 
cicatricial strictures, fecal impaction, and sometimes intussusception. In 
many cases, however, in which the obstruction is chronic, that is, in which 
the narrowing of the lumen develops and progresses slowly, symptoms 
may for a long time be absent, and ultimately develop suddenly, that is, 
clinically the obstruction is acute. 

Acute intestinal obstruction is characterized by abdominal pain, 
tenderness, nausea, vomiting, constipation, tympanites, and occasionally 
a palpable abdominal tumor. Pain is usually an initial symptom, comes 
on suddenly, is acute and colicky in nature, though after the obstruction 
is complete it generally becomes continuous, and is always very severe. 
In the early hours of the attack, at least, it is commonly associated with 
active (visible and audible) peristalsis. It is not always localized to 



678 DISEASES OF THE INTESTINE 

the site of the obstruction, but may be referred or diffuse; and it is 
often associated with abdominal tenderness, which also may be diffuse. 
Nausea and vomiting follow soon upon the pain, and are sometimes the 
most distressing symptoms, especially when associated with hiccough, 
which is not uncommon. The vomit consists at first of the stomach 
contents (usually food), then (second or third day) of greenish, bile- 
stained fluid, and ultimately (third, fourth, or fifth day), if the obstruction 
is complete and the patient is not relieved, of brownish-black, feculent 
or stercoraceous material — an important diagnostic feature. At the 
onset of the obstruction, or soon thereafter, the bowels may be opened — 
a discharge of the feces below the obstruction; but otherwise, in a great 
majority of cases, constipation is absolute, neither feces nor gas being 
discharged, though in a few cases the incessant tenesmus may result in 
the passage of a little mucus, and in intussusception there may be both 
blood and mucus. Tympanites is a feature of almost all cases, coming on 
after the lapse of twenty-four hours. It varies much in degree in dif- 
ferent cases, being marked in obstruction of the large bowel, but often 
slight if the small bowel high up is involved. Rarely an abdominal 
mass may be palpable, especially in intussusception or fecal impaction, 
but in many cases the exquisite tenderness and pain preclude satisfactory 
examination. The examination, however, in obscure cases may be 
facilitated by anesthetization, and a rectal or vaginal exploration may 
furnish conclusive evidence. 

The constitutional symptoms are always severe. The expression is 
anxious, the face pallid and bathed in cold sweat, the eyes sunken, the 
pulse rapid and feeble, and soon evidences of collapse supervene. The 
temperature is usually subnormal, unless peritonitis develops. The urine 
is diminished, sometimes greatly diminished, and may contain an excess 
of indican (especially in obstruction of the small intestine), and later 
some albumin. Leukocytosis, sometimes of high degree, is usually 
present. If not relieved, the patient usually dies, soon after the third 
day, with manifestations of peritonitis and auto-intoxication — delirium, 
coma, muscular twitchings, fever, etc. 

Chronic intestinal obstruction varies somewhat symptomatically, 
depending upon the cause of the obstruction. Cicatricial or cancerous 
obstruction is characterized by long-standing and increasing constipation, 
alternating sometimes with attacks of diarrhoea, and frequently associated 
with colicky pains. The pains, however, often occur at long intervals and 
are usually attributed to indigestion. The masses of formed fecal matter 
are sometimes observed to diminish progressively in caliber, but one 
must remember that fecal masses narrowed by passing through a stric- 
ture may acquire ordinary size and contour in the rectum. There is often 
a sensation of fulness in the abdomen, tympanites develops and is not 
uncommonly associated with active peristalsis (visible and audible), 
which often furnishes remarkably trustworthy evidence of how far down 
the bowel is patulous. Vomiting may occur, but is rather unusual and 
rarely fecal in character. Attacks of more or less complete, though 



INTESTINAL OBSTRUCTION 679 

temporary, obstruction, due to accumulation of feces above the con- 
striction, may occur from time to time, and are sometimes attended by 
fever, due doubtless to auto-intoxication. Intestinal hemorrhage is 
occasionally observed. In some cases a more or less definitely de- 
limitable mass is palpable — usually in the region of the cecum or the 
sigmoid, but sometimes elsewhere. The patient, as a rule, fails in 
general health, becomes anemic and cachectic, and ultimately dies from 
asthenia or, not infrequently, from the consequences of acute obstruction. 

In obstruction due to fecal impaction the symptoms, for the most 
part, are quite similar to the foregoing; constipation is of long stand- 
ing, but channelling of the fecal masses may permit the discharge of 
mucus or watery stools. Subjective symptoms are for a long time, in 
many cases, notoriously slight, despite even great accumulation; but in 
some cases, abdominal pain and distention may be complained of. When 
the obstruction is complete the pain and distention are more marked, and 
vomiting may supervene and even become feculent. Rectal examina- 
tion, as well as examination along the course of the colon, may disclose 
scybalous masses, which have a peculiar putty-like consistency and 
may be somewhat moved about. 

Diagnosis. — The diagnosis is concerned with (1) the seat of the 
obstruction, (2) the nature of the obstruction, and (3) the differentiation 
from other conditions that may give rise to similar symptoms. 

The seat of the obstruction is sometimes impossible of certain deter- 
mination, but it may be surmised by attention to the age and sex of 
the patient (having reference to what has already been said in this con- 
nection), and by bearing in mind the slightly less frequency, more sudden 
onset, more acute course, more severe local and general symptoms, more 
common feculent and protracted vomiting, more likely suppression of 
urine, excessive indicanuria (due to decomposition of the intestinal con- 
tents), and the early development of peritonitis, in obstruction of the 
small intestine. Obstruction of the small intestine is also suggested by 
uniform distention of the central portion of the abdomen, with slight or 
no distention of the lateral portions (situation of the colon), and active, 
visible, palpable, and audible peristalsis (transverse or oblique ridges). 
In obstruction of the beginning of the jejunum the distention and peri- 
stalsis may be slight and limited to the upper part of the abdomen, or 
may be altogether absent; but vomiting, gaseous eructations, and hic- 
cough are likely to be marked, and collapse comes on early. In obstruc- 
tion of the beginning of the duodenum, the symptoms are similar to 
those of stenosis of the pylorus; in obstruction of the duodenum below 
the diverticulum of Vater, pancreatic juice may be present in the vomit 
(but it may be absent in disease of the pancreas, such as carcinoma of 
the head, which itself may be the cause of the obstruction). Obstruction of 
the large intestine, if due to strangulation, may quite simulate obstruc- 
tion of the small intestine, but otherwise it is suggested by slower devel- 
opment of ■ the symptoms of occlusion; less rapid course; later develop- 
ment and less frequency of vomiting which is less likely to be feculent; 



680 DISEASES OF THE INTESTINE 

limitation of the initial distention and peristalsis to the colon (horse- 
shoe curve, but frequently irregularly developed); palpable tumor or 
fecal masses along the course of the colon; more tenesmus with discharge 
of mucus and blood; less likelihood of anuria; and the later development 
of peritonitis. A rectal or vaginal examination should not be neglected. 
In obstruction of the small intestine high up empty and collapsed intes- 
tines may be found in the pelvis; in some cases of volvulus of the sigmoid 
the rectum may be distended (paralytic distention), but contain no feces; 
and in intussusception the descending intestine may be palpable in the rec- 
tum. Some observers have advocated rectal exploration with the entire 
hand, and if the hand be lady-like this may not be devoid of service. 
Indefinite or well-defined masses (tumors or fecal masses) may be 
palpable through the abdominal wall in some cases, even despite con- 
siderable tympany, but is much facilitated by anesthetization. Some- 
times assistance is obtained by inflating the rectum and the colon with 
air or distending it with water, the point where the inflation ceases, or 
the amount of water that may be introduced, suggesting the seat of the 
obstruction; or after the introduction of air or of bismuth paste a radio- 
graphic examination may disclose the seat of obstruction. Sometimes, 
as suggested by Treves, auscultating while inflating or distending the 
bowel may afford evidence of the seat of obstruction. 

The nature of the obstruction sometimes cannot be diagnosticated,, 
but help may be obtained by attention to the age and sex of the patient, 
an examination of the palpable openings (for hernia), a rectal or vaginal 
examination, and the clinical history of the case — acute or sudden onset; 
an injury to the abdominal wall; previous peritonitis, pelvic or otherwise, 
localized, or diffuse (suggesting bands or adhesions causing compression 
or traction); the ingestion of a foreign body; previous gallstone colic; 
chronic constipation; symptoms of stenosis of the bowel; general failure 
of health, with the development of anemia, emaciation, and cachexia 
(suggesting carcinoma), etc. Intussusception is more readily recognized 
than other conditions : it occurs especially in children, is of sudden onset 
(sometimes following diarrhoea), is attended by tenesmus and bloody and 
mucous discharges, and occasionally through the abdominal wall, in the 
course of the colon (especially the transverse), a peculiar, usually sausage- 
shaped mass, may be palpable, and may even become hard and firm 
(contracted) under the hand; in other cases it may be felt through the 
rectum. Volvulus and strangulation, except in so far as they are suggested 
by adult life, can rarely be recognized with certainty before operation. 
Fecal impaction, and in many cases malignant stenosis, should readily 
be distinguished. 

Conditions resembling symptomatically intestinal obstruction are 
often difficult of differentiation. Internal hernias (obturator, diaphrag- 
matic, internal inguinal ring, etc.) can rarely be distinguished. Other 
conditions which may occasion confusion are acute appendicitis, acute 
pancreatitis, acute peritonitis, acute enteritis (especially in children), 
intestinal colic, gallstone colic, nephritic colic, torsion of the pedicle 



INTESTINAL OBSTRUCTION 681 

of an ovarian or uterine tumor or of a floating kidney, a phantom tumor, 
etc. In many cases of acute obstruction peritonitis develops so promptly 
as to be really part and parcel of the disease. In these, as well as in 
other cases, the diagnosis cannot go beyond acute obstruction. 

Prognosis. — The prognosis varies, depending upon the nature of the 
obstruction, and in many cases upon the promptness ol appropriate 
treatment. In acute obstruction the prognosis is always grave, a fatal 
termination occurring usually in from three to seven days unless the con- 
dition is relieved. In chronic obstruction symptoms are often present for 
months, until, as in carcinoma, the patient eventually dies of asthenia, or 
rather suddenly from acute obstruction. When due to fecal impaction 
recovery usually follows clearing of the bowel. In the event of certain 
complications, such as gangrene, perforation, peritonitis, etc., the outlook 
is practically hopeless. 

Treatment. — A knowledge of the pathological conditions present in 
intestinal obstruction suggests the futility of medicinal treatment in 
all but the exceptional case, and in this the fortunate outcome is often 
the result rather of good luck than of good management. Excepting only 
fecal impaction, intestinal obstruction is essentially a surgical disease 
and should be treated on surgical principles. Since in many cases it is 
impossible to differentiate between the different forms of intestinal ob- 
struction, and since delay only adds to the danger, operation should be 
undertaken with the least possible delay. 

Pending the advent of the surgeon, the stomach should be washed out 
repeatedly with warm saline solution — a mode of treatment warmly 
advocated by Kussmaul and others, and tending to relieve not only the 
persistent vomiting, but also the intestinal distention and pressure above 
the obstruction, and thus mitigate the violent peristalsis and the pain. 
Irrigation of the rectum and colon is also of much service in some cases 
and may occasionally, especially in intussusception in children, result 
in the reduction of the intussusception — though it is not wise to expect 
this as a necessary result of the treatment. The amount of fluid injected 
should be measured with a view to determine the distance of the obstruc- 
tion from the anus. Under no circumstances whatever should purgatives 
be administered; even in fecal impaction they should not be given until, 
after repeated and copious oil or watery enemas, the major portion of the 
impacted feces has been discharged. 

The question of the use of opium before operation has been much 
debated. Personally, I prefer not to use it, if it can be avoided. In some 
cases, however, the pain is really intolerable, and if it cannot be relieved 
by hot or cold applications externally and atropine internally, morphine 
may be given in small dose — the smaller the better, since in the event of 
operation its deleterious effects may become only too apparent. Recently 
a number of good results have been reported from the use of atropine in 
very large doses, -fa to y 1 ^- grain (0.002 to 0.005 gram) twice or thrice 
in the first twenty-four hours ; the pain has been relieved and spontaneous 
recovery has resulted. The treatment merits further trial. 



682 DISEASES OF THE INTESTINE 

That some patients have withstood repeated and even forcible dis- 
tention of the rectum and colon, drastic cathartics, violent shakings, 
strenuous kneading of the abdomen, etc., merely illustrates the wonder- 
ful resources of the human economy; and that some patients have suc- 
cumbed to this treatment (production of perforation, etc.) rather than to 
the disease, as such, cannot well be doubted. Personally, I should prefer 
the chances of operation, in what is admittedly a very serious disease, 
to the hazard and hope of medicinal treatment. 



DILATATION OF THE COLON. 

Dilatation of the colon may be due: (1) Gaseous accumulation, 
which, though usually transitory, is of significance from the fact that from 
pressure upward it may seriously embarass the action of the heart and 
lungs, particularly if these organs are diseased. (2) Fecal accumulations, 
with which gallstones, enteroliths, and foreign bodies may be associated. 
(3) Obstruction of the colon, usually carcinomatous or a volvulus; 
less commonly cicatricial stricture, sigmoid diverticulitis, etc. (4) 
Idiopathic dilatation of the colon (Hirschsprung's disease; Virchow's 
giant growth of the colon). This is usually congenital and is seen in 
children in more than three-fourths of the cases. There may be stricture 
of the sigmoid, but usually there is no apparent obstruction. The 
colon may attain really a giant growth, as in Formad's case, in which 
it measured 15 to 30 inches in circumference, and with the contained 
feces weighed 47 pounds. The chief symptoms are obstinate and pro- 
longed constipation, alternating, perhaps, with periods of diarrhea, 
markedly protuberant abdomen, especially in the course of the colon, 
and in some cases visible colonic peristalsis. The disorder is intract- 
able, auto-intoxication, emaciation, in some cases complete intestinal 
obstruction, peritonitis, etc., eventually ensuing. Treatment is unsatis- 
factory. Treves has successfully removed the greater part of the colon. 



INFARCTION OF THE MESENTERIC VESSELS. 

Embolism of 'the mesenteric arteries (most commonly the superior 
mesenteric artery) may occur in arteriosclerosis, vegetative endocarditis, 
aneurysm, etc. Thrombosis of the mesenteric veins may follow directly 
on infections, especially ulcerative process in the intestine (appendicitis, 
intestinal ulceration), or it may develop secondarily in cirrhosis of the liver, 
pylephlebitis, and anemic and cachectic states; and it usually follows 
arterial embolism. Gangrene of the supplied part of the intestine follows ; 
if the area blocked is small, an efficient collateral circulation may be 
established, but if the superior mesenteric artery (virtually an end-artery) 
is involved, death is inevitable. The symptoms are usually abrupt in 
onset, and consist of sudden abdominal pain, nausea, vomiting, and 
bloody diarrhoea. Soon peritonitis sets in, and the patient usually 



HEMORRHOIDS 683 

succumbs within two or three days. In a few cases the onset is more 
insidious and the symptoms not necessarily obtrusively intestinal. The 
diagnosis is rarely made with certainty. It may be suspected in the 
event of endocarditis or aneurysm, which may furnish the obstructing 
embolus. Usually the diagnosis is intestinal obstruction. Operation 
and resection of the gangrenous bowel is occasionally successful; other- 
wise treatment is unavailing. 

INTESTINAL SAND. 

Of conditions described as intestinal sand there are two — the true and 
the false. True intestinal sand (intestinal lithiasis) consists of small, 
usually dark-colored, gritty particles formed of an organic base, but 
made up largely of inorganic salts (often 75 per cent, or more), especially 
calcium phosphate and carbonate. It is more frequent in women (two- 
thirds of the cases) than in men, especially in nervous and hypochondriacal 
subjects, between the thirtieth and the fortieth year. 

Etiology. — The process of the formation of true intestinal sand has been 
likened to that of appendicular calculi and gallstones. Duckworth and 
Garrod believe that since the sand contains only traces of unaltered bile 
pigment and no cholesterin (distinction from gallstones) and is rich in 
urobilin, it must be formed in the upper part of the colon, where the 
conversion of bile pigment into urobilin is well advanced, and which is 
structurally better adapted than the small intestine for the lengthy sojourn 
necessary for the deposition of earthy salts. False intestinal sand is 
made up of the residue of certain articles of food and occasionally of 
medicines. The sclerenchymatous particles of pears (pear sand), par- 
ticles of bananas, seeds of fruits (figs and different berries), fish bones, 
grain residues, etc., have been observed as forming so-called intestinal 
sand. Olive oil, in consequence of partial digestion, has been known 
to form masses resembling gallstones (whence the erroneous opinion 
as to the efficacy of the olive oil treatment), and substances like salol 
may also give rise to so-called (false) intestinal sand. 

Symptoms. — Clinically the discharge of the sand is usually attended by 
more or less, sometimes very severe, colicky pain, due to constipation or 
to mucous colic (with which it is often associated). Clinically, as a rule, no 
pain attends the discharge of false intestinal sand, any pain complained 
of being likely due to constipation, for the relief of which, figs, etc., may 
have been taken. 

Treatment. — The treatment is that of the associated conditions, such 
as intestinal colic, constipation, and mucous colic. 

HEMORRHOIDS. 

{Piles; Hemorrhoidal Phlebectasis.) 

Etiology. — Hemorrhoids, or varicose dilatations of the inferior hemor- 
rhoidal veins, is a purely local disease, due to mechanical obstruction of the 



684 DISEASES OF THE INTESTINE 

circulation, and is caused by: (1) Local disease of or about the rectum, 
such as fecal accumulation, rectal inflammations, strictures and tumors 
of the rectum or adjacent structures (uterus, ovary, bladder, prostate, etc.); 
(2) obstruction to the portal circulation due to cirrhosis and other dis- 
orders of the liver and portal system; and (3) chronic passive congestion 
due to heart disease. Sedentary occupations, repeated pregnancies, 
straining at stool, etc., are believed to act as contributing factors. 

Pathology. — Hemorrhoids may be external or internal, or both. In- 
ternal hemorrhoids are in close relation with the sphincter, but some- 
times they extend high up in the rectum, and even into the sigmoid. 
External hemorrhoids may consist of (a) a, small venous tumor, that 
develops suddenly (in consequence of rupture of one of the external 
hemorrhoidal veins), is dark purplish in color, and very tender; (b) 
small tabs of skin and connective tissue, which originally contained some 
more or less dilated and tortuous veins. They may be single or multiple, 
pedunculated or sessile, and not infrequently surround the anus. They 
rarely occasion symptoms. Internal hemorrhoids may be (a) diffuse, 
that is, thickened, dilated, tortuous, and closely aggregated venous cords 
and capillaries (sometimes also arterioles) ; usually granular on inspection, 
and covered with a very thin and readily torn mucous covering — whence 
the frequent bleeding (bleeding piles); (6) circumscribed tumor masses, 
single or multiple, roundish or irregular in outline, and more or less 
encircling the bowel. They may be pedunculated or have a broad base 
of attachment; they are bright red when inflamed, and dark reddish or 
purplish when much congested or filled with clot (due to rupture of a 
vessel). They may become extruded, and in consequence partially or com- 
pletely strangulated by the sphincter, or ulcerated, and give rise to more 
or less hemorrhage. 

Symptoms. — Small and even moderately large hemorrhoids often exist 
without occasioning any symptoms, though examination may reveal their 
presence. Symptoms, when present, vary with the number, size, and 
condition of the hemorrhoids. Probably the commonest complaints are 
sensations of discomfort, sometimes a more or less constant desire to 
evacuate the bowel, a temporary dissatisfied sensation following defe- 
cation, and anal itching and burning. Defecation is often painful, some- 
times so painful as of itself to engender voluntary constipation. The 
final evacuation of the hardened feces only induces more severe pain, and 
eroding the piles provokes more or less abundant hemorrhage. When 
the piles are inflamed, ulcerated, or strangulated, blood and mucus may 
pass from the bowel altogether independently of the stools. Sometimes 
a high grade of secondary anemia is induced; hypochondriasis and 
melancholia are by no means uncommon. 

Diagnosis. — External piles are readily recognized by inspection; internal 
piles necessitate digital exploration or protoscopic examination for their 
recognition. 

Prognosis. — Since the causes of hemorrhoids are so largely chronic, 
their course is usually progressive. In themselves they are not fatal, 



VISCEROPTOSIS 685 

except in so far as neglect may lead to serious and even fatal complica- 
tions, such as strangulation and gangrene. 

Treatment. — The treatment is either palliative or curative. The curative 
treatment is surgical — ligation or excision — and may be resorted to in the 
great majority of cases. Many patients, however, will not submit to 
operation, and an operation may be ill advised in subjects with advanced 
heart or liver disease. Marked benefit may usually be secured in many 
cases by securing a daily evacuation of the bowels, by habits of regularity, 
attention to the diet, and saline aperients if necessary. Local cleansing 
is of the utmost importance. Applications of ice water or of an ice 
bag, or even a cold sitz baljh after the daily evacuation, is of benefit. 
Local pain and itching may be relieved by belladonna, ichthyol, or 
iodoform (by suppository), by the fluid extract of hamamelis, or by 
equal parts of gall and belladonna ointment. In other cases excellent 
results follow the use of iron subsulphate, 2 to 3 grains (0.13 to 0.20 
gram) by suppository, or a 10 to 15 per cent, ointment. Intractable 
hemorrhage, ulceration, strangulation, etc., call for surgical intervention. 



VISCEROPTOSIS. 

(Splanchnoptosis; Enleroptosis; Gastroptosis; Coloptosis; Hepatoptosis; Nephroptosis; 
Splenoptosis; Glenard's Disease). 

Visceroptosis is an inclusive term used to describe the condition in 
which the abdominal viscera fall from their normal to a lower position 
in the abdomen. The stomach, intestine, transverse colon, and the 
kidneys are most commonly involved, but any or all of the abdominal 
viscera may "drop" in the individual case. 

Etiology. — Two causative factors are operative — a congenital weak- 
ness or laxity of the mesentery and ligament supporting the abdominal 
organs, and lack of the normal support afforded by the abdominal wall. 
The majority of cases occur in women, in whom, in consequence of 
repeated pregnancies, ill-fitting and tightly laced corsets, etc., the ab- 
dominal wall becomes lax and flaccid. In both sexes factors like trau- 
matism, excessive muscular strain, such as may be associated with 
chronic constipation and severe coughing, emaciation, recurring ascites, 
etc., may lead to the disorder. In some, especially young subjects, there 
seems to be undoubtedly a congenital weakness of the supporting liga- 
ment and mesentery, since there is often no undue laxness of the abdom- 
inal wall. 

Pathology. — Visceroptosis in itself is, perhaps, not to be looked upon 
as a disease sui generis; aside from their abnormal position, the organs 
may be quite normal. 

Symptoms. — Several classes of cases may be encountered. In the one, 
even considerable grades of ptoses may exist without notable symptoms. 
In a second series of cases, obviously due to a markedly relaxed abdomen 
(repeated pregnancies), there may be more or less marked symptoms. 



$86 DISEASES OF THE INTESTINE 

In a third series, the conspicuous symptoms are neurasthenic (nervous- 
ness, headache, backache, asthenia, anemia, emaciation, etc.), with spe- 
cial complaints directed to the gastro-intestinal tract. These comprise, 
as a rule, the more common manifestations of indigestion, such as poor 
or capricious appetite, epigastric pain and distress, gaseous and acid 
eructations, flatulence, nausea, and constipation; in some cases there 
is hyperacidity, in others motor insufficiency. Examination reveals the 
stomach dropped, in toto, the lower border two or three inches or more 
below the umbilicus, and the upper border correspondingly ptosed: a 
depression in the epigastrium and a fulness about the umbilicus. The 
stomach is usually more vertical than normally, especially in women 
who have laced tightly; and it may also be dilated. Waves of peristalsis 
may be visible, but they are much weaker than those due to organic 
obstruction; occasionally, however, considerable pyloric obstruction 
may be caused by malposition of the pylorus, perigastric adhesions, a 
displaced right kidney, etc. The intestines, also, especially the colon, 
may be much displaced. The transverse colon may fall as low as the 
brim of the pelvis, occasioning a so-called V- or M-shaped colon; and 
the sigmoid may be markedly redundant: in both cases constipation is 
usually a marked symptom. 

Ptosis of one or both kidneys, usually the right, is often associated with 
gastro-enteroptosis, but it may occur independently thereof. There is 
usually more or less pain in the lumbar region, or a sense of weight and 
dragging; it may be so severe as to simulate and be indistinguishable 
from renal colic; or it may be a part of Dietl's crises: severe pain, chills, 
fever, nausea, vomiting, and collapse; the urine is usually lessened in 
amount and may contain blood and pus, and the kidney may be en- 
larged and tender. The cause of these crises is not well understood; 
they have been attributed to twists or kinks of the renal vessels or ureters, 
obstruction of the bowels, etc. On examination, the kidney, when 
ptosed, may be just palpable on deep inspiration, which is quite common, 
especially in women and on the right side, and is not of much conse- 
quence; it may be so movable that on deep inspiration it descends to 
about the level of the umbilicus, and may be retained there by the pal- 
pating hand during expiration; or it may be floating, quite low, and 
readily pushed about to or beyond the median line, in the iliac fossa, etc. 

Ptosis of the liver and spleen is much less common, and may be readily 
recognized by physical exploration. 

Diagnosis. — The diagnosis is readily made upon physical examination. 
The most trustworthy results follow radiographic examination, in the 
case of the stomach and intestine, after inflation with air or bismuth 
paste. Some diagnostic importance has been ascribed by Stiller to a 
floating tenth rib, which he believes the most common stigma of the basic 
congenital asthenic condition; but a floating tenth rib occurs under other 
circumstances. 

Prognosis. — The outlook as regards relief of symptoms and improve- 
ment in the general health is good. One must remember that even con- 



DISEASES OF THE LIVER 687 

siderable degrees of ptosis may be present without notable symptoms. 
So long as the motor power of the stomach, for instance, is efficient, 
symptoms may be entirely in abeyance. 

Treatment. — The underlying neurasthenic condition demands the 
most careful attention — hydrotherapy, regulated feeding, general tonics 
(especially nux vomica), change of scene and air, etc. Gastric hyper- 
acidity or subacidity, flatulence, and constipation must be treated, as 
mentioned under these headings. Much relief may be afforded by a 
properly made, fitted, and applied bandage or abdominal supporter; in 
fact, the bandage in itself may lead to symptomatic cure. Occasionally 
resort may be had to operative measures — to elevate a markedly dis- 
placed stomach or colon, to resect a redundant sigmoid, etc. 



DISEASES OF THE LIVEE. 

Pathological Physiology. — The functions of the liver are: To detoxify 
poisons that enter the body by way of, or are elaborated within, the 
gastro-intestinal tract, or are perhaps produced elsewhere; to secrete bile; 
to warehouse some of the excess of fat taken as food and to release it 
when the supply from without becomes deficient; to warehouse gly- 
cogen derived from the carbohydrates taken as food, or from the non- 
nitrogenous part of the proteins when the supply of carbohydrates is 
deficient, and to convert the glycogen into glucose and liberate it as it 
is required by the system; and to assist in the metabolism of the pro- 
teins, to the extent, at least, of forming urea from ammonia compounds. 
There are other functions, such as erythrocytolysis, etc., that are of 
minor interest in the present connection. 

Disorder of the functions of the liver may be primary or secondary; 
and it may be partial, involving perhaps only one function, or it may be 
total, involving presumably all the functions. The belief in a primary 
general disorder of function is well exemplified in the terms torpid liver, 
biliousness, bilious headache, lithaemia, etc. Present-day opinions tend, 
perhaps unwisely, to minimize the influence of the liver in these disorders; 
but this seems an almost inevitable result of the knowledge that phe- 
nomena commonly attributed to a supposed torpid liver and the other 
affections mentioned may result from factors that do not involve the 
liver primarily, if at all, and that uric acid (lithemia), by no means the 
important factor in disease it was once thought, is not formed exclusively 
in the liver. The dyspeptic symptoms of a supposed torpid liver are 
usually due to a gastro-intestinal catarrh set up by dietetic indiscretions, 
excessive eating (especially of proteins and carbohydrates), the con- 
sumption of too much alcohol, etc.; the spread of this catarrh to the 
diverticulum of Vater and the common bile duct, or perhaps rarely a 
toxic descending radicular cholangitis, is answerable for the subicteric 
tint of the conjunctiva and skin common in these subjects; and the head- 
ache and other nervous symptoms result from the absorption and circu- 



688 DISEASES OF THE LIVER 

lation in the blood stream of enterogenic toxins. The liver usually 
participates in the process only secondarily; perhaps the enterogenic 
toxins are produced in such amounts that the liver is incapable of neu- 
tralizing them and they pass over into the circulation, or they are so 
virulent that they impair the functional activity of or set up congestive 
and other alterations in the liver. In either event the symptoms are 
gastro-intestinal rather than hepatic in origin, and the liver, responding 
to excessive demands and being in consequence actively congested, is 
often, for a time at least, of increased rather than of decreased func- 
tional activity. The bearing of these facts on treatment is obvious and 
material. 

There is, however, another series of cases, such as the passive con- 
gestion of chronic cardiac and pulmonary disease, in which there is reason 
to believe that the functional activity of the liver is reduced. It is not 
unlikely that the headache and other nervous symptoms, digestive dis- 
turbances, and loss of flesh and strength that occur in these cases are 
due, in part at least, to the disordered functions of the liver. This is 
perhaps due directly to the influence of enterogenic poisons which, being 
carried to the liver by the portal circulation, encounter an organ reduced 
in vitality by the long-continued passive congestion, and incapable of 
exerting as it should its detoxifying function; the toxins, in consequence, 
pass over into the general circulation and cause at least some of the 
symptoms. 

In another series of cases, more or less complete functional failure of 
the liver ensues. These are cases of severe intoxication or infection, in 
which widespread destruction or disorganization of the hepatic paren- 
chyma occurs. The striking clinical phenomena, which may develop 
suddenly, although they are sometimes preceded by minor symptoms, 
are for the most part nervous; they are variously designated hepa tarsia, 
acholia, cholemia, hepatic auto-intoxication, etc. Headache is a con- 
spicuous symptom, and is soon followed by mental excitement, delirium 
(which may be very active or maniacal), muscular twitchings, and con- 
vulsions; or mental hebetude progressing to deep coma may ensue. 
Most of these cases are associated with varying grades of jaundice and 
other phenomena that will be more fully discussed under jaundice and 
acute yellow atrophy of the liver. 

Disturbances in the detoxifying function of the liver is believed by 
some observers to be the basis of the eclamptic manifestations of uremia, 
pregnancy, etc. Disorder of the fat metabolism often leads to acidosis 
and acid intoxication, due to the presence of acetone, diacetic acid, and 
/?-oxybutyric acid in the blood. These substances are formed princi- 
pally in the liver and the muscles, but probably also in other tissues. 
They result from imperfect oxidation and are directly related to deficient 
glycogen in the liver and muscles — which may be the consequence 
of insufficient intake (as in starvation), or of excessive output (as in 
diabetes). ^ 

Alimentary levulosuria has been suggested as a test of the functional 



JAUNDICE 

capacity of the liver, and is perhaps of some diagnostic significance in 
cirrhosis. The test should be performed as follows: Food should be 
withheld after the evening meal until the test has been completed. In 
the morning the patient should void his urine, and then (upon an empty 
stomach) he should take 100 grams of levulose dissolved in 500 c.c. of 
water. Weak tea without cream may be substituted for the water if pre- 
ferred by the patient. At the end of an hour, and hourly thereafter for 
four hours, the patient should void his urine. The specimens should be 
examined separately for levulose, preferably by the polariscope, or by the 
Seliwanoff method, which is as follows: Equal parts of the urine and 
of a half-and-half solution of concentrated hydrochloric acid and water 
should be mixed in a test-tube, and a few grains of resorcin added. The 
mixture should then be boiled, whereupon, if levulose is present, a beau- 
tiful red color appears ; this deepens on standing and a dark-red deposit 
settles in the test-tube. If the disorder of the liver be of moderate 
severity, the levulose will be found in the third or fourth specimen of 
urine, perhaps in the fourth only; if there be profound alteration of the 
hepatic structure, the levulose may be found in the first specimen of 
urine, as well as in the subsequent specimens, and it may persist for 
several additional hours. 

JAUNDICE. 

Jaundice is a term applied to staining of the tissues with bile pigments 
— bilirubin and biliverdin. It is merely a symptom, and is recognized 
clinically by a yellowish or yellowish-green discoloration of the skin and 
visible mucous membranes and by the presence of bile pigment in the 
urine. 

Types of Jaundice. — Jaundice can result only from: (1) An obstruction 
somewhere in the course of the biliary tract, in consequence of which the 
free flow of the bile being impeded, it becomes absorbed by the lymphatics 
or bloodvessels — jaundice from stasis of bile; or (2) disturbances in the 
functions of the liver cells, whereby the bile is diverted from the biliary 
capillaries to the lymphatics or the blood channels — jaundice from para- 
pedesis of bile. In the one case the disorder involves the bile after it 
has been formed and entered the biliary channels; in the other it involves 
the bile pigments while they are still within the hepatic cells. 

Obstructive or Mechanical Jaundice. — In the event of obstruc- 
tion to the extrahepatic or intrahepatic biliary ducts the outflow of bile is 
hindered, while the hepatic cells still continue to secrete bile, so that the 
biliary ducts, even to the finest biliary radicles (capillaries), become 
often enormously dilated. Finally, the biliary capillaries rupture into the 
lymph spaces between the hepatic cells and the bloodvessels; thence by 
way of the lymphatic vessels and the thoracic duct the biliary constituents 
reach the blood stream and the tissues of the body. This type of jaun- 
dice may be found in cases of: (1) Obstruction within the common bile 
duct or the hepatic duct; such as gallstones, parasites, foreign bodies, 
44 



690 DISEASES OF THE LIVER 

etc.; (2) inflammatory, cicatricial, or neoplastic stenosis of the ducts; 
(3) compression of the ducts from without by tumors of the pancreas, 
stomach, intestine, gall-bladder, regional lymph nodes, kidney, retro- 
peritoneum, mesentery, etc., inflammatory adhesions, swollen lymph 
nodes, fecal accumulations, aneurysm of the aorta or of the hepatic or 
mesenteric artery, etc.; (4) kinking or torsion of the ducts the conse- 
quence of gastroptosis, hepatoptosis, nephroptosis, the pregnant uterus, 
tumors of the abdominal or pelvic organs, etc; and (5) diseases of the 
liver unattended by gross obstruction of the extrahepatic biliary ducts, 
such as localized inflammatory processes (abscesses), tubercles, gummas, 
hydatid cysts, primary and secondary newgrowths within the substance 
of the liver, etc. 

Hemolytic, Toxic, Infectious, Hemohepatogenous Jaundice. — 
Cases of jaundice in which no obstruction of the biliary ducts can be 
found were formerly described as non-obstructive or hematogenous, 
in contradistinction to the obstructive or hepatogenous cases. But 
Naunyn, Minkowski, Stadelmann, and others definitely proved that 
all jaundice is hepatogenous — in the sense that bile pigments are 
formed only in the liver. Since, however, in many cases increased 
destruction of erythrocytes provides the material (hemoglobin) from 
which the bile pigments are formed in excess (polychromia), these cases 
are sometimes spoken of as hemohepatogenous jaundice; and since they 
occur in toxic, infectious, and other conditions associated with increased 
hemolysis, they are spoken of as hemolytic, toxic, or infectious jaundice. 

The mechanism of this type of jaundice is not well understood. 
Frerichs believed that the bile found its way directly into the blood- 
vessels, in consequence of changes in the tension of the contents of the 
hepatic cells and of the bloodvessels — either an increase in the inter- 
cellular pressure or a decrease in the portal pressure. Liebermeister 
believed that the disordered liver cells lost their ability to retain or fix the 
bile, and that in consequence it became diffused into the bloodvessels or 
lymphatics — so-called diffusion or akathektic jaundice. Minkowski 
assumed a disturbance in the normal currents within the liver cells, so 
that the bile became diverted from the biliary capillaries to the blood- 
vessels or lymphatics — jaundice from parapedisis (paracholia of Pick). 
It is probable that the toxic and infectious causes of this form of jaundice 
seriously compromise the functional integrity of the liver cells; but it 
has also been demonstrated that they provoke also a radicular cholan- 
gitis— which obstructs the free flow of bile. Eppinger states that in 
these cases thrombi made up of coagulated bile occur in and obstruct the 
biliary capillaries; in consequence thereof, mechanical stasis of the bile 
develops in the finest biliary capillaries, and, as in cases of gross obstruc- 
tion of the larger extrahepatic ducts, the biliary canaliculi dilate and 
ultimately rupture into the pericellular lymph spaces. In these cases 
there is at first an increased formation and excretion of bile (polycholia) 
and of bile pigments (polychromia, pleiochromia) ; soon, however, the 
excretion of bile lessens, the bile that is excreted becomes viscid, and 



JAUNDICE 691 

finally excretion may cease — which may be attributed to a radicular cho- 
langitis or the biliary thrombi, or both. Thus, although this form of 
jaundice is properly called toxic, infectious, or hemolytic, it is at the same 
time hepatogenous and obstructive. 

This hemolytic jaundice occurs in many infections, such as the different 
types of so-called infectious jaundice, syphilis, yellow fever, septico- 
pyemia, malaria, pneumonia, typhoid fever, etc.; in intoxications, such 
as poisoning with ptomaines, phosphorus, arseniuretted hydrogen, chlo- 
roform, mushrooms, toluylenediamin, pyrogallol, snake venom, coal-tar 
products, etc.; in acute yellow atrophy of the liver; occasionally in cir- 
rhosis and other diffuse diseases of the liver; in progressive pernicious 
anemia and hemoglobinemia; in disturbances of the circulation, such as 
passive congestion; in certain nervous perturbations (so-called emo- 
tional jaundice, menstrual jaundice, both of more than doubtful occur- 
rence); in the newborn; and as a chronic family or hereditary disorder. 

In a number of cases, in addition to the jaundice, there are phenomena 
of general infection, such as fever, neuromuscular pains, enlargement of 
the spleen and liver, gastro-intestinal disorders, such as vomiting and 
diarrhoea, nervous manifestations, such as headache, stupor, etc., often 
leukocytosis, albuminuria, tube casts, etc.; to these cases the term in- 
fectious jaundice (Weil's disease) has been applied. The not uncom- 
mon epidemic occurrence of such cases warrants the use of the term 
epidemic jaundice. In other cases the clinical phenomena are more 
severe, symptoms attributable to hepatic insufficiency (hepatargia), to 
poisoning by bile acids (cholemia), or to hepatic auto-intoxication (acid- 
osis), supervene, and a fatal issue usually ensues; the condition is spoken 
of as grave jaundice (icterus gravis). When, in addition, considerable 
destruction of the liver cells occurs, the term acute yellow atrophy of the 
liver is employed. No sharp line of distinction can be drawn between 
these cases; cases mild in the beginning may progress to the most severe 
and fatal (acute yellow atrophy); and the degree of jaundice bears no 
constant relationship to the demonstrable changes in the liver, nor to 
the severity of the other clinical phenomena. 

Icterus neonatorum is a peculiar form of jaundice that develops in from 
two-thirds to three-fourths of newborn infants on the second or third day 
of life, and usually fades within a week or ten days. The cutaneous dis- 
coloration is slight, and is commonly unattended by other symptoms. The 
urine is often of normal color, and usually does not contain soluble bile 
pigments, but may reveal biliary granules or crystals in desquamated renal 
epithelium. The nature of this form of jaundice is not well understood. 
It has been attributed to compression of the biliary capillaries by dis- 
tended portal radicles; to catarrhal cholangitis (Virchow); and to biliary 
stasis in consequence of the diminutive size of the bile ducts and conse- 
quent obstruction (Kehrer and Cohnheim). Frank attributed it to 
absorption of bilirubin from the meconium; and Quincke has suggested 
that this bilirubin, which is not converted into urobilin on account of 
the absence of intestinal fermentation in the newborn, being absorbed, 



692 DISEASES OF THE LIVER 

reaches the general circulation by way of the ductus venosus without 
traversing the liver. Most likely it is really due to the erythrocytolysis 
of the early days of life; that is, it is hemolytic in nature. This benign 
form of jaundice must be distinguished from a more severe and fatal form 
that may also occur in the early days of life in consequence of congenital 
syphilis, septicopyemia, WinckePs disease, congenital obliteration of the 
bile ducts, etc. 

Chronic family jaundice (hereditary jaundice, congenital hemolytic 
jaundice, acholuric jaundice, splenomegalic jaundice, hemolytic ictero- 
anemia) is a form of chronic non-obstructive jaundice (first accurately 
described by Minkowski) that is usually hereditary or occurs in several 
members of the same family, although some cases are "acquired/' It 
may date from birth or develop during adolescence; and it usually lasts 
for years without notable impairment of the general health. Its chief 
characteristics are slight or moderate jaundice, enlargement of the 
spleen, well-colored stools, the presence of urobilin and urobilinogen 
in the urine (but no bile pigments), moderate anemia, and occasional 
attacks of fever, of biliousness (following dietetic indiscretions), and of 
epigastric pain, etc. (due to complicating gallstones). Itching, slow 
pulse, multiple hemorrhages, xanthelasma, and other usual accompani- 
ments of jaundice are commonly absent. The disease is due to increased 
fragility of the erythrocytes, or their decreased resistance to hemolyzing 
agents (Chauffard). In the differential diagnosis one has sometimes to 
take into consideration all the aforementioned types of jaundice occurring 
soon after birth, as well as (in older subjects) Hanot's biliary cirrhosis — 
which occasionally occurs in several members of the same family. 

Effects of Jaundice. — All of the tissues and organs, with the exception 
of the nervous, are stained with biliary pigments; and in some severe 
cases of toxic or infectious jaundice the nervous system also may be 
stained. The staining is due, in part, to the deposition of biliary pig- 
ments in the tissues, in part to the circulation of blood and lymph con- 
taining undeposited pigments. It is most marked in the skin, mucous 
membranes, serous membranes (endocardium, intima of vessels, etc.), 
the liver, kidneys, heart, sweat, serous transudates, exudates, etc. The 
saliva, tears, mucus, and milk are not stained unless an inflammatory 
exudate be added to them. 

Jaundice is manifested first by a yellowish discoloration of the con- 
junctivae; in mild cases the discoloration is demonstrable there only. 
The skin becomes of a characteristic lemon-yellow, orange-yellow, 
greenish-yellow, olive, or olive-bronze color. The discoloration is light 
in many cases of toxic or hemolytic jaundice, in which it is rarely more 
than moderate in grade; it is light also in mild cases of catarrhal cho- 
langitis; it is darkest incases of permanent and complete obstruction of 
the common bile duct, and it may become so dark — olive bronze or 
greenish black — as to warrant the designation black jaundice (melan- 
icterus, icterus melas). The intensity of the jaundice in these cases is 
proportionate to the completeness of the obstruction of the common 



JAUNDICE 693 

duct, or, in case the obstruction involve one of the larger intrahepatic 
ducts, to the size of the duct implicated. Pruritus is common and dis- 
tressing; rarely it precedes the discoloration of the skin. Urticaria and 
considerable sweating (often localized to the palms) are sometimes ob- 
served. Local infections, such as boils, occasionally occur. In chronic 
cases, local telangiectases of the skin (sometimes also of the oral and 
other mucous membranes) tend to develop, and flat or nodular yellowish, 
chamois-leather-colored patches (xanthelasma, xanthoma, vitiligoidea) 
may appear on the skin or mucous membranes. 

Bradycardia is a characteristic feature, especially of acute cases and 
those of short duration. The pulse rate may fall to 60, to 40, even to 
21 (Frerichs) a minute, and it is subject to sudden fluctuations upon 
slight provocation. This has been attributed to a local inhibitory action 
of the bile acids on the cardiac muscle or ganglia; but recent investiga- 
tions suggest that perhaps the action is on the central nervous system. 

Bile pigments are present in excess in the circulating blood, but whether 
they exert any deleterious effect on the blood itself has not been satis- 
factorily determined. The clotting time of the blood is much increased 
— from the normal three to four minutes to ten to twelve minutes — a fact 
of much importance when surgical operations in jaundiced patients are 
under consideration. In protracted and severe cases there is a marked 
tendency to subcutaneous, submucous, and subserous hemorrhages. 

In jaundice a considerable portion of the biliary derivatives is excreted 
in the urine, which, in consequence, is discolored yellowish, yellowish 
red, greenish, or greenish-brown, depending upon the relative amounts 
of bilirubin, biliverdin (its oxidation product), or urobilin (its reduction 
product). These bile pigments may be found in the urine several hours, 
sometimes even several days, before there is any obvious discoloration 
of the skin or visible mucous membranes; they constitute, thus, the 
first clinical manifestation of jaundice. In addition, the urine often 
contains a number of hyaline, sometimes bile-stained, casts — attributable 
to irritation of the convoluted and Henle's tubules provoked by excreting 
the bile pigments (which are not excreted by the glomeruli). In other 
and particularly long-standing cases, in addition to casts, the urine is 
diminished in amount, of increased specific gravity, and contains more or 
less albumin — an expression of nephritis due probably to associated toxic 
conditions rather than to the jaundice per se. Urobilin and urobilinogen 
are commonly found in the urine. They are formed in the intestine by 
the action of bacteria on bilirubin; they are absorbed and carried to the 
liver by the portal circulation. Some diagnostic significance has been 
attached to their presence, as well as that of phenol, in the urine in disease 
of the liver. The occurrence of urobilinuria in cases of jaundice, how- 
ever, does not justify the designation " urobilin jaundice," since the 
cutaneous pigmentation is due to bilirubin and biliverdin. 

The functions of the liver, in addition to the formation of bile, may be 
disturbed — reduction in the glycogen content and lessening of the detoxi- 
fying function. The liver cells are sometimes much degenerated, not 



694 DISEASES OF THE LIVER 

always, however, directly in consequence of the jaundice. Eppinger has 
shown that in these cases marked regenerative changes occur to replace 
cells destroyed. In advanced cases of obstructive jaundice pericho- 
langitic fibrosis sometimes occurs, and has been described as a form of 
biliary cirrhosis. The absence of bile from the intestinal tract results in 
the passage of large, pale, grayish, slate-colored or clay-colored, pasty, 
fetid acid stools. The pale color is due, in part only, to the absence of 
bile; in part it is due to the large amount of imperfectly digested fats, 
which may be increased from the normal 7 to 10 per cent, to as much as 
SO per cent. Microscopically and chemically the fats are found to con- 
sist of free fatty-acid crystals and soaps (calcium and magnesium) of the 
higher fatty acids; neutral fats are present in very small amounts. 
Rarely pale or decolorized stools contain biliary derivatives in consider- 
able amounts — determinable by chemical examination; this occurs espe- 
cially in disease of the pancreas attended by obstruction to the outflow 
of the pancreatic juice, but unassociated with jaundice. The pale color 
of the feces in these cases is due to the large amount of fat, and to the 
reduction of bilirubin to leukourobilin. Constipation is the rule, but 
sometimes the bowel movements are frequent, perhaps diarrhceic, which 
may be due to large fecal masses resulting from imperfect digestion of 
fat and to the laxative action of the free fatty acids. 

Grave disturbances of the nervous system occur in many cases of 
jaundice; on the one hand, there are manifestations of depression, such 
as general neuromuscular weakness, asthenia, headache, vertigo, mental 
depression (that may progress to melancholia), insomnia, etc.; on the 
other hand, there are manifestations of irritation, such as severe head- 
ache, active delirium, coma, convulsions, etc. These manifestations are 
more common in cases of acute toxic or infectious jaundice (associated 
with fever) than in the more protracted cases of obstructive jaundice; 
but they may supervene in any case of jaundice and not uncommonly 
lead to the fatal issue. They are commonly described under the name 
cholemia, but it is difficult to separate from one another the symptoms 
due to bile acidemia, to interference with the detoxifying function of the 
liver, and to the initiating toxic or infectious process. The condition 
is not cholemia in a restricted sense — that is, it is not due to bile acidemia, 
since the symptoms may occur when bile acids are not in excess in the 
blood, as well as in cases of disease of the liver (such as cirrhosis) unas- 
sociated with jaundice. The condition is most likely an acid intoxication, 
due to disturbances of the detoxifying function of the liver, which may be 
brought about by disorganization of the hepatic parenchyma. Xan- 
thopsia and hemeralopia also are probably due to a toxic disturbance of 
the retina, rather than to the sometimes assumed discoloration of the 
media of the eye. 

Man is able to withstand the effects of jaundice for a long time. The 
fatalities that ensue in the acute, as well as in the chronic, cases are due not 
so much to the jaundice per se as to other causes — the underlying cause 
of the jaundice, acid intoxication, etc. In long-standing cases, however, 



ANOMALIES OF FORM AND POSITION 695 

more or less disturbance of the general nutrition gradually ensues — due 
largely to imperfect fat absorption. To supply sufficient calories to pre- 
vent breaking down of the body tissues, there must be considerable 
increase in the protein intake; this results in loss of appetite, disordered 
digestion, perhaps diarrhoea, etc., so that, the intake being reduced, the 
patient must utilize his own fat or protein tissue to cover the continued 
loss, and, having no means of restoring the deficit, a very dangerous 
inanition results. 



ANOMALIES OF FORM AND POSITION. 

Congenital Anomalies of Form.— The liver, in consequence of 
defects of development, is occasionally found in the thoracic cavity or pro- 
jecting beneath the skin near the umbilicus (hepatomphalos) ; in mon- 
sters the organ may be entirely absent. In partial and complete transpo- 
sition of the viscera the liver may be as much in the left half of the body 
as normally it is in the right; in this event the left lobe is the larger. 

Acquired Anomalies of Form (Deformities). — The important 
acquired anomalies of form consist of (1) the so-called corset or constricted 
liver; and (2) linguiform lobulation. The corset or constricted liver is the 
consequence of tight lacing, and is therefore almost wholly confined to the 
female sex (as much as 25 per cent, of female cadavers in some series); 
but an analogous condition is sometimes encountered in men, the result 
of the constricting influence of a tight belt or strap. The basis of the 
deformity is a pressure atrophy of the liver parenchyma followed by 
fibrosis. Sometimes there is only a deep circumferential furrow; usually 
the liver is considerably elongated and markedly thinned at the point of 
greatest constriction (most marked atrophy), which often corresponds 
with the plane of the upper pole of the right kidney. Various grades of 
this condition are encountered, and it gradually merges into that spoken 
of as linguiform (or RiedeVs) lobe (partial hepatoptosis). This also is 
common in female subjects, but it is intimately related to cholelithiasis 
and cholecystitis, enlargement of the gall-bladder being found in 60 per 
cent, of the cases. These linguiform lobes are often long and much 
attenuated; frequently they are attached to the main portion of the liver 
by a thin fibrous band; and they are often extremely mobile (partial 
hepatoptosis). The corset liver and a linguiform lobe may be entirely 
symptomless. In some cases there are symptoms of indigestion, as likely 
due to the tight lacing per se as to the changes in the liver. A lingual 
lobe is sometimes painful and tender, due to congestion or associated 
cholecystitis and cholelithiasis; occasionally nausea and vomiting ensue, 
and have been attributed to interference with the functions of the pylorus 
and duodenum; occasionally pains of biliary colic occur. In other cases 
the abnormality of the right lobe is detected accidentally, and may be 
mistaken for an abdominal tumor. 

Treatment. — The corset liver is better prevented than cured. The 
symptoms attributable to a linguiform lobe are most amenable to the 



696 DISEASES OF THE LIVER 

surgical measures appropriate to the cure of cholecystitis and cholelithi- 
asis, to which they are largely due. 

Acquired Anomalies of Position. — The liver may be displaced 
upward, downward, or laterally, or it may be rotated on its antero- 
posterior axis (anteverted or retroverted), usually the result of disease 
of adjacent thoracic or abdominal organs. 

The important acquired anomaly of position is that variously spoken of 
as hepatoptosis, wandering liver, movable liver, etc., a condition in which 
the liver is abnormally movable and presents variously in the abdominal 
cavity. It is mentioned in connection with visceroptosis (page 685). 



DISEASES OF THE BLOODVESSELS OF THE LIVER. 

Hepatic Artery. — Dilatation is observed in cirrhosis and other condi- 
tions when the portal vein is obstructed. Thrombosis is very rare. Em- 
bolism occasionally occurs; it may be mechanical, infectious (provoking 
multiple abscesses), or sarcomatous (usually melanotic from the eye). 
Aneurysm is rare (40 cases). The chief symptoms are pain, jaundice, 
and hemorrhage into the alimentary tract. 

Hepatic Veins. — Dilatation occurs in chronic heart disease attended 
by failure of the right ventricle. Thrombosis is rare, but may occur in 
various sorts of disease in and about the vein. The lesions are analogous 
to those of chronic passive congestion. It may be suspected in cases of 
aggravated passive hyperemia upon the sudden onset of ascites. Em- 
bolism (retrograde embolism) occasionally occurs from reversal of the 
blood current, due to vigorous contraction of the right ventricle, cough- 
ing, sneezing, and other violent expiratory efforts, and the forces of 
gravity. The lesions vary with the nature of the embolus (mechanical, 
infectious, neoplastic). Suppurative phlebitis may occur in pyogenic 
infections of the liver. Chronic obliterating hepatic endophlebitis is rare. 
The condition resembles and is usually mistaken for cirrhosis. 

Portal Vein. — Dilatation is part of portal cirrhosis, and is attributable 
to increased blood pressure. Thrombosis (pylethrombosis, pylephle- 
bitis adhesiva) is rather common in cirrhosis of the liver and in intra- 
abdominal newgrowths, but it may occur also in inflammatory disorders 
of the abdominal viscera. The thrombosis may begin in the portal 
radicles within the liver, in the main trunk of the vein, or in the peripheral 
radicles anywhere within the area of collection of the vein; and subse- 
quently, by extension, the process may become widespread. In some 
cases the disorder seems to be due to a low-grade infection. The portal 
vein may become converted into a fibrous cord (pylephlebitis adhesiva), 
and a collateral circulation may become established. The diagnosis is 
rarely possible, but is suggested by sudden onset of ascites of high grade, 
gastro-intestinal hemorrhage, enlargement of the spleen, abdominal pain, 
and symptoms of intestinal obstruction. Death may occur soon; at all 
events, usually within two years. The treatment is palliative; the ascites 



FATTY LIVER 697 

may require repeated tapping. Embolism of the intrahepatic branches of 
the portal vein is a common sequence of inflammatory, suppurative, ulcer- 
ative, and neoplastic processes in the organs within the area of collection 
of the portal vein. Suppurative pylephlebitis is common, especially in 
early adult life, and, like adhesive pylephlebitis, may begin in the portal 
radicles within the liver, in the main trunk of the vein, or in the peripheral 
radicles anywhere within the area of collection of the vein; and subse- 
quently, by extension, the process may become more or less widespread. 
Usually the disorder is secondary to ulcerative or suppurative processes of 
the gastro-intestinal tract, especially appendicitis, dysenteric and other 
ulcerations of the intestine, etc. The infecting microorganisms are 
staphylococci, streptococci, Bacillus coli, Bacillus dysenterise, etc. The 
symptoms consist of those of the antecedent disorder, to which are grad- 
ually added (if they have not already existed) irregular chills, fever, 
sweats, polynuclear leukocytosis, and prostration; as well as extension of 
abdominal pain beyond the seat of original disease, enlargement and 
tenderness of the liver, perhaps also of the spleen, and sometimes vomit- 
ing, hematemesis, and diarrhoea. Usually the patient soon passes into 
a typhoid state and dies. Chronic portal endophlebitis rarely occurs : as 
a primary disease (syphilis, splenic anemia with sequential Banti's dis- 
ease, etc.), or as a secondary process (chronic passive congestion and 
cirrhosis of the liver). Partial or complete thrombosis may follow. 

FATTY LIVER. 

Fatty liver is a comprehensive term applicable to the different con- 
ditions characterized by an excess of fat in the liver. It includes fatty 
infiltration, in which there is an excessive deposit of fat in otherwise unal- 
tered or slightly altered liver cells; and fatty degeneration, in which, in 
addition to the fat, there are greater or less degenerative changes in the 
hepatic parenchyma, perhaps the direct conversion of the liver cells into 
fat. Formerly the two conditions were differentiated; doubtless there 
are extreme cases of fatty infiltration and of fatty degeneration, but many 
cases partake of the nature of both processes, and, contrary to former 
opinions, there is now considerable trustworthy evidence to suggest at 
least that the fat in the liver under all circumstances is derived mainly 
from adipose tissue elsewhere in the body. 

Etiology. — The causes of fatty liver are: (1) Dietetic indiscretions and 
the disorders of metabolism that tend to produce obesity, of which fatty 
liver (mostly infiltration) is a conspicuous feature; (2) anemic and ca- 
chectic conditions, such as occur in the late stages of tuberculosis, amyloid 
disease, carcinoma, etc.; (3) passive congestion; (4) poisons, such as 
alcoholism, phosphorus, arsenic, antimony, chloroform, etc; (5) certain 
local infections of the intestinal tract, such as the gastro-intestinal catarrh 
of children, dysentery, etc. ; (6) certain general infections, notably strep- 
tococcic, staphylococcic, and other pyococcic infections of long dura- 
tion (prolonged suppuration), tuberculosis, etc. 



698 DISEASES OF THE LIVER 

Pathology. — Usually the liver is enlarged, and may weigh 3000 to 4000 
grams; it is of lessened specific gravity (sometimes floating in water), 
and of lessened resistance; it is normal in conformation, and has a smooth 
surface and rounded edges, and is pale yellowish in color. Histologically, 
fatty infiltration and degeneration may be combined in varying propor- 
tions. 

Symptoms. — The symptoms of fatty liver are ill defined. In general, 
the symptoms are those of the primary disorder-obesity, tuberculosis, 
alcoholism, toxemic conditions, etc. In perhaps the majority of cases 
there are no symptoms referable directly to the liver; occasionally sensa- 
tions of weight may be due to the mere weight of the liver, and ill-defined 
dyspeptic symptoms may be attributed to functional inactivity of the 
liver, although they are more likely to be due to associated disorders of 
the stomach and intestines, improper eating and drinking, etc. The 
liver is enlarged and commonly palpable two or three fingers' breadth 
below the costal margin. 

In phosphorus poisoning the early symptoms are those of gastro- 
intestinal irritation (epigastric distress, nausea, and vomiting). If the 
patient does not die soon, there is commonly a period of quiescence, that 
to the unwary suggests recovery and speedy cure. At the end of two or 
three days, however, vomiting and epigastric distress return, jaundice 
supervenes, the pulse becomes weak and accelerated, the heart dilated, 
subcutaneous, submucous, and subserous hemorrhage develop, and the 
patient usually dies within a week. In most cases the liver is enlarged 
throughout, smooth and tender; in some cases it decreases in size before 
death. 

Diagnosis. — Minor grades of fatty liver cannot be recognized with cer- 
tainty; the more marked grades must be differentiated from other causes 
of enlargement, such as the fatty cirrhotic liver, amyloid liver, leukemic 
infiltration, passive congestion, displaced liver, etc. 

Prognosis. — The prognosis depends upon the primary cause. 

Treatment. — The treatment is altogether that of the primary disorder. 



ACUTE YELLOW ATROPHY OF THE LIVER. 

Acute yellow atrophy of the liver is an acute, widespread autolytic 
necrosis of the liver cells, characterized clinically by jaundice, reduction 
in the size of the liver, and toxic disturbances of cerebration, proceeding to 
a fatal issue. 

Etiology. — Acute yellow atrophy of the liver is especially frequent be- 
tween the twentieth and thirtieth year (50 per cent, of the cases), and in 
women (two-thirds of the cases). Both of these facts are explainable 
largely by the frequent occurrence of the disease during pregnancy; 
almost if not quite one-half of the cases in women occur about the middle 
or during the latter half of pregnancy. The causative influence of preg- 
nancy is akin to that exerted by the toxemia of pregnancy, in which the 



ACUTE YELLOW ATROPHY OF THE LIVER 699 

liver frequently shows degenerative changes, and in the production of 
which it plays an important, if not the important, part. Various known 
infections exert some etiological influence; thus 10 per cent, of the 
cases occur during secondary syphilis (in which slight jaundice is not very 
rare); pyogenic infections (septicopyemia, osteomyelitis, erysipelas, etc.), 
typhoid fever, malaria, diphtheria, etc., may antedate the liver disorder. 
Etiological significance is also attributed to certain non-bacterial poisons, 
such as alcohol, ptomaines, chloroform, phosphorus, etc. Chloroform is 
of undoubted significance, being responsible for the cases of so-called 
delayed chloroform poisoning. Phosphorus gives rise to a somewhat 
analogous condition, but the lesions in the liver are not alike in the two 
disorders. Similar phenomena may develop in the course of other dis- 
eases of the liver, such as advanced passive congestion, cirrhosis, cholan- 
gitis, etc. All of the foregoing leads to the conclusion that the designa- 
tion acute yellow atrophy, as well as icterus gravis, comprises a series of 
diverse disorders that exhibit more or less superficial resemblance. We 
are now able to separate some of the cases from the main group, such as 
those due to syphilis, septicopyemia, puerperal eclampsia, phosphorus 
poisoning, delayed chloroform poisoning, etc., but the definite etiological 
factor of the major group is still unknown. 

Pathology. — The liver is much reduced in size and weight, being often 
one-half or one- third that of the normal (800 to 500 grams or less). The 
organ is flaccid and has so lost its normal elasticity and resistance that 
it may be folded or bent upon itself. On sectioning the liver it is found 
to be dense and resistant; the section surface is mottled — yellowish or 
yellowish-red areas of varying size and configuration alternating and 
more or less gradually merging the one into the other. The yellowish 
coloration is due chiefly, if not entirely, to bilirubin rather than to fatty 
alterations (the fat content is usually not increased, and may be dimin- 
ished) ; the reddish areas seem to be an advanced stage of the yellow, and 
to be more numerous or larger the longer the patient lives. Examination 
of the fresh liver tissue (scrapings of the section surface) reveals necrotic 
liver cells, erythrocytes, leukocytes, leucin, tyrosin, and xanthin. Histo- 
logically there is intense and widespread (not focal) destruction of the 
liver cells. Ultimately the cells disappear, apparently in consequence 
of autolysis, and leave behind the supporting framework of the liver, 
granular debris, and endothelium of the capillaries (the reddish areas on 
macroscopic inspection). The small bile ducts become obstructed in 
consequence of desquamation of their lining epithelium and participate 
in the production of the jaundice. In some, especially protracted, cases 
there are conspicuous evidences of attempts at regeneration (compen- 
satory hyperplasia) of the liver cells; pseudobiliary canaliculi derived 
from the liver cells as well as the smaller bile ducts also are often con- 
spicuous. All the organs are more or less bile-stained. The spleen is 
soft, and is slightly or moderately enlarged in about two-thirds of the 
cases. The kidneys are enlarged, softened, pale, opaque, and often 
reveal small foci of hemorrhage, cloudy swelling, and fatty changes. 



700 DISEASES OF THE LIVER 

Small hemorrhages are found beneath the skin and the various serous 
membranes (pleura, pericardium, peritoneum, meninges) and mucous 
membranes (gastro-intestinal, respiratory, and genito-urinary tract), and 
are doubtless attributable to toxic changes in the blood and blood- 
vessels. 

F. W. White supports the view, originally advanced by Flexner, that the 
process is autolytic in nature, and that it is brought about by some poison 
having a specific action on the liver cells whose life it destroys without 
injuring the proteolytic ferments they contain, whence autodigestion 
ensues. The leucin and tyrosin result partly from autolysis of the liver, 
and partly from non-conversion into urea of leucin and tyrosin formed 
elsewhere. Other evidence of this autolysis is found in the albuminose 
(decomposing protein) and purin bodies (destruction of nuclein) some- 
times encountered in the urine. The reduction in the excretion of urea 
and the increased excretion of ammonia are interpretable as efforts on 
the part of nature to neutralize increased acidosis, whence the process 
may be looked upon as an acid intoxication. White believes that the 
chief symptoms of the severe intoxication are due largely to the damage 
done to the functions of the liver, and that the special poisonous sub- 
stances are probably: (1) Nitrogenous antecedents of urea; (2) certain 
products of decomposition in the bowel which are normally deprived of 
their toxic power in passing through the liver; and (3) decomposition 
products of the destroyed liver tissue; and, further, that this view is borne 
out by observation of other severe diseases of the liver in which little 
or no jaundice occurs. 

Symptoms. — The initial symptoms are those of gastro-intestinal catarrh, 
soon (one to four days) followed by jaundice; these may last a variable 
period, usually five to seven days, but sometimes several weeks. During 
this period the disorder is usually looked upon as ordinary catarrhal 
jaundice (cholangitis), and as a matter of fact there is little if anything to 
suggest the more serious disorder. The patient complains of malaise, 
perhaps fugitive neuromuscular pains, poor appetite, coated tongue, occa- 
sional vomiting, constipation, etc. ; there is usually moderate jaundice and 
bile pigment in the urine. Soon, however, the graver symptoms super- 
vene. The jaundice deepens, becoming dark yellowish or bronze-like, 
slightly greenish (in rare, extremely rapid cases jaundice may be absent); 
severe nausea and vomiting set in and are often associated with hema- 
temesis; diarrhoea may supervene; and grave nervous symptoms ensue 
— headache, mental confusion, hebetude, and restlessness, soon followed 
by a noisy delirium, and later coma and perhaps convulsions. Hemor- 
rhages (disordered nutrition of the vessel walls and hemolytic action of bile 
salts on the erythrocytes) occur beneath the skin and into and from divers 
mucous membranes (intestines, urinary tract, respiratory tract, genital 
tract, retina, and most commonly the stomach); abortion may occur in 
pregnant women. Soon the patient passes into a profound typhoid 
state. There may be slight fever (pyococcic infection), but usually the 
temperature is below normal (until shortly before death, when there may 



ACUTE YELLOW ATROPHY OF THE LIVER 701 

be an agonal rise); the pulse becomes rapid, feeble, and of low tension; 
the respirations become accelerated and irregular; the pupils dilate (said 
to be important, diagnostically) ; the tongue becomes dry, furred, and 
tremulous; sordes collect on the teeth and gums; and there are fibrillary 
twitchings of the muscles, etc. 

The liver in some cases is found slightly or moderately enlarged in the 
early days of the disorder; this may be due to preexisting disease (as cir- 
rhosis), but rarely it seems to be a part of the acute yellow atrophy itself. 
Soon, however, the liver dulness diminishes rapidly in extent, until it may 
be entirely absent or constitute a small area in the axillary region. Slight 
or moderate enlargement of the spleen may be made out in about two- 
thirds of the cases. 

The feces, as a rule, are dark and offensive. The dark color in the 
early stages is that of normal feces; that of the feces late in the disease is 
probably due, in part at least, to contained blood, which obscures the 
paucity of the bile, since very little if any bile probably enters the intestine 
in the advanced stages of most cases. The stools may be light colored, 
especially if there be diarrhoea. 

The urine, as a rule, is lessened in amount, of increased specific gravity, 
of increased acidity, and high colored (bile pigment and excess of uro- 
bilin); it usually contains a small amount of albumin, and hyaline, 
granular, fatty, and epithelial tube casts. The highly significant changes 
consist in the presence of leucin, tyrosin, and the other amino-acids 
(largely the result of autodigestion of the liver); sarcolactic, diacetic, and 
other fatty acids (lactic, acetic, butyric, and succinic); marked reduction 
in the amount of urea with an associated increase in the amount of am- 
monia and other nitrogenous substances. A moderate leukocytosis (up 
to 16,000) may be present. Occasionally there may be ascites. 

Diagnosis. — Careful studies of the urine, especially in pregnant women, 
and in cases of mild jaundice, and the detection of significant urinary 
changes, especially evidences of an acid intoxication, should enable us 
to recognize the antecedent conditions and perhaps ward off the more 
serious later stages. The development of nervous symptoms in any case 
of jaundice should always awaken suspicion. When fully developed, 
jaundice, vomiting, delirium (and other cerebral symptoms), lessening in 
the size of the liver, and the presence of leucin and tyrosin in the urine 
are unmistakable (although leucin and tyrosin may be found in other 
conditions). 

Phosphorus poisoning may be excluded by the absence of a history of 
the ingestion of phosphorus (not always trustworthy), the latter develop- 
ment of jaundice (which in phosphorus poisoning usually supervenes 
after a day or two of symptoms referable to disordered stomach), decrease 
in the size of the liver (which usually remains enlarged in phosphorus 
poisoning), the more severe nervous symptoms, and the constant occur- 
rence and larger amounts of leucin and tyrosin. The liver of phosphorus 
poisoning may contain 30 per cent, of fat, as contrasted with 5 per cent, 
in acute atrophy. 



702 DISEASES OF THE LIVER 

Prognosis. — The disease is almost invariably fatal. A few cases of 
recovery have been reported. 

Treatment. — In the early stages the patient should be confined to bed. 
Milk is the best food, and should be diluted with some alkaline mineral 
water; cereals and other carbohydrates may be given in considerable 
amounts, since they are likely to prevent or limit the acid intoxication. 
The bowels should be opened freely and repeatedly, with a view to 
remove all noxious matters from the intestine, as well as material from 
which toxic substances may be formed ; calomel and the saline cathartics 
seem the best. Insistence should be laid upon the drinking of large 
amounts of an alkaline water. Alkaline diuretics and other alkalies 
(sodium bicarbonate) and enteroclysis and hypodermoclysis may be 
resorted to. Intestinal antiseptics are indicated theoretically. Stimu- 
lants, such as alcohol, strychnine, and digitalis, are useful for the general 
vital depression and collapse; an ice-cap to the head, the bromides inter- 
nally, and a warm bath or sponge, or a small amount of morphine (^- to 
■^q grain, 9.002 to 0.006 gram) or of cocaine (^ grain,0.008 gram) hypo- 
dermically, may control the restlessness and delirium; warm applications 
to the abdomen, and cocaine, dilute hydrocyanic acid, bismuth, and car- 
bolic acid, or small amounts of champagne, etc., may control the vomiting. 

ACTIVE CONGESTION OF THE LIVER. 

Etiology. — Active congestion of the liver, usually toxic in nature and 
gastro-intestinal in origin, may result from: (1) The processes of diges- 
tion, when it is a normal condition; (2) endogenous and exogenous 
poisons that may be carried by the portal vein (alcohol, overeating, 
ptomaines, bacterial toxins, etc.); (3) bacterial toxins that may reach the 
liver by way of the general circulation (typhoid fever, malaria, pyococcic 
infections, etc.); (4) "cold," "a chill upon the liver," the "tropical 
liver;" and (5) perhaps vasomotor disturbances (menstruation, etc.). 
Most of these factors are the causes also of inflammation and degener- 
ative changes in the liver; it is difficult, if not impossible, to separate the 
one set of conditions from the other; they are often combined. 

Symptoms. — The cases associated with dietetic indiscretions are 
manifest by so-called indigestion, or the complex popularly designated 
"biliousness" (poor appetite, coated tongue, epigastric distress, nausea, 
occasionally vomiting, constipation, headache, etc.). Perhaps there 
is a sub icteric hue to the sclerse and the skin; the liver may be found 
slightly enlarged and tender. In the cases met in infections, such as 
dysentery, malaria, etc., the constitutional symptoms are more marked; 
slight or moderate fever is usually present (progression to acute hepa- 
titis); and the local gastro-intestinal symptoms may be more or less in 
abeyance, although they may become aggravated during digestion. The 
liver becomes enlarged and tender. 

Diagnosis. -The diagnosis is usually apparent from the etiological 
factors, the general disturbances of the gastro-intestinal tract, the slight 



PASSIVE CONGESTION OF THE LIVER 703 

jaundice, and enlargement and tenderness of the liver; by no means 
of minor diagnostic importance is recurrence of attacks in a person of 
known ill-chosen habits of eating and drinking. The diagnostic diffi- 
culties consist in determining whether or not to the congestion permanent 
damage to' the liver tissue has been added. With recurrence of attacks, 
their increasing duration, and lessening intervals, this becomes the more 
likely. In the more acute cases encountered in infections, aggravation 
of the constitutional symptoms, together with enlargement and tender- 
ness of the liver, usually suffice for diagnosis. In these cases there are 
usually parenchymatous changes in addition to the congestion. 

Prognosis. — The disorder rarely lasts more than three or four days; 
sometimes a week. It is not dangerous in itself, but acquires its impor- 
tance because of its etiological factors (especially alcohol) and its fre- 
quent recurrence in the indiscrete: in those that persist in the use of 
alcohol, in whom it is likely to eventuate in cirrhosis; and in those con- 
tinuously exposed to other etiological factors, such as malaria, dysentery, 
etc., in the tropics, in whom freedom from recurrences can only be 
obtained by removal to temperate zones (freedom from etiological 
causes). 

Treatment. — The treatment is that of acute non-suppurative hepatitis. 



PASSIVE CONGESTION OF THE LIVER. 

Etiology. — Passive congestion of the liver, largely mechanical in nature 
and cardiac in origin (whence, cardiac liver), occurs : (1) In acute and 
chronic failure of the heart, the ultimate condition in myocardial, peri- 
cardial, and chronic valvular disease; (2) in advanced stages of such 
diseases of the lungs as cause increased work of the right side of the heart 
and finally lead to its failure (chronic bronchitis, emphysema, chronic 
adhesive pleuritis, etc.); and (3) from local factors that obstruct the cir- 
culation about the junction of the hepatic veins and the inferior vena cava 
(kyphosis, inflammatory adhesions, angulation by a displaced heart, 
pleural effusion, etc.). 

Pathology. — Three stages of passive congestion of the liver may be 
distinguished: (1) The merely congested or engorged liver, found in 
cases of acute or recent heart failure (common in infections, such as 
pneumonia, typhoid fever, etc.), and in chronic valvular disease, with 
well-maintained compensation, in which death has occurred suddenly 
or after a few days' illness only; (2) the congested nutmeg liver, found in 
cases of long-standing heart disease, with dilatation of the right heart 
and tricuspid insufficiency, in which compensation, although precari- 
ously maintained, has been on the whole fairly satisfactory, and in which 
no serious or prolonged failure has occurred until that which leads to 
death; and (3) the fibrotic nutmeg liver (red atrophy of the liver), found 
also in cases of long-standing heart disease with dilatation of the right 
heart and tricuspid insufficiency, in which one or more severe and pro- 



704 DISEASES OF THE LIVER 

longed attacks of failure of compensation have occurred, during which 
likely the auricle has suffered especially, and, being perhaps totally inca- 
pacitated, has permitted the full force of the ventricle to be transmitted 
to the hepatic lobules with consequent rupture of the venules and capil- 
laries, laceration and destruction of hepatic parenchyma, and its repair 
by newgrown connective tissue (scar tissue). It is likely that congestion 
of the liver in the early stages of cardiac failure (whether due to endo- 
cardial, myocardial, pericardial, or pulmonary disorder) is a compen- 
satory process; that this is especially active in acute failure, such as 
occurs in many infections and in the early stage of chronic valvular disease; 
that not until the liver has been distended to and beyond its capacity 
does oedema ensue; and that with the progress of th valvular defect and 
the gradual loss of the safety-valve action of the liver oedema appears 
more and more easily. 

Symptoms. — The symptoms consist of those due to the primary cardiac 
or pulmonary disease, especially dyspnoea, cyanosis, and oedema, and 
those due more directly to the disorder of the liver itself. These com- 
prise especially pafn and distress or a sense of weight and heaviness 
in the right hypochondrium, and gastro-intestinal phenomena, such 
as poor appetite, epigastric distress especially after eating, flatulence, 
nausea, and constipation. These are due in part to general venous en- 
gorgement, in part to portal congestion transmitted from the congested 
hepatic veins. Slight or moderate jaundice is common; the admixture 
of the jaundice and more or less cyanosis gives to the patient a very char- 
acteristic bluish or purplish, green or yellow discoloration. (Edema, 
followed by ascites, is often present, being part of the cardiac decom- 
pensation. Occasionally the ascites is disproportionately large in 
amount and may require repeated tappings; in this event it is associated 
with the flbrotic congested liver or with chronic adhesive peritonitis 
(perihepatitis). The liver is enlarged, perhaps reaching to or below the 
transumbilical line; it is tender, and it may reveal an expansile ven- 
tricular systolic pulsation. 

Diagnosis. — The diagnosis is usually evident from a knowledge of the 
primary disorder, an enlarged and tender liver, and other evidences of 
failing cardiac compensation. 

Prognosis. — The prognosis is altogether that of the primary disorder. 

Treatment. — The treatment is that of the primary cardiac or pul- 
monary disorder; virtually it is that of failing cardiac compensation. 

PERIHEPATITIS. 

Acute Perihepatitis. — Acute perihepatitis is almost if not always a 
secondary disorder, due to antecedent disease of the liver or adjacent 
viscera. The lesions may be localized or diffuse, and fibrinous, sero- 
fibrinous, or purulent in character. The fibrinous exudation may 
undergo organization and lead to filamentous or dense adhesions; the 
suppurative lesions may be part of one form of subphrenic abscess. 



ACUTE HEPATITIS 705 

The important symptoms consist of local pain and audible and palpable 
frictions. There may be a short, hacking cough (perhaps set up by 
manipulation of the liver), hiccough (suggesting involvement of the 
diaphragm), and nausea and vomiting. The diagnosis is often obscured 
by the predominance of the symptoms of the primary disorder. The 
treatment is that of the primary disease and local measures (strapping, 
counterirritation, etc.) to relieve the pain. Operation is required in the 
suppurative cases. 

Local Chronic Perihepatitis. — Local chronic perihepatitis usually 
follows and is therefore due to the same causes as the acute process. The 
lesions are usually quite firm adhesions that serve to bind the neighboring 
organs variously to one another. The symptoms are scarcely, if ever, 
definite, but local pain, tenderness, and rigidity may suggest the disorder. 

General chronic perihepatitis will be discussed under diseases of the 
peritoneum (multiple serositis, page 750). 

ACUTE HEPATITIS. 

Acute Non-suppurative Hepatitis. — The term acute nonsuppu- 
rative or parenchymatous hepatitis is employed to include a series of 
most diverse disorders that exhibit all stages of progression from acute 
congestion to the inflammatory focal necroses of many infections, and 
the more widespread process manifested clinically as the different forms 
of icterus gravis and acute yellow atrophy of the liver. Manifestly the 
term is not strictly applicable to all of these. 

Etiology. — The causes of acute congestion of the liver already men- 
tioned may cause acute non-suppurative hepatitis; the difference be- 
tween these disorders is one of degree only. As a matter of fact, acute 
hepatitis is uncommon in temperate climates. In the tropics, however, 
a disorder described by those of experience as acute parenchymatous 
hepatitis (tropical liver) is of frequent occurrence; it is most commonly 
provoked by malaria, but also by dysentery and perhaps other infections. 
It occurs especially in young adult Europeans, and not uncommonly soon 
(during the first year) after their arrival in the tropics. Undoubtedly 
factors other than malaria and dysentery are active in the etiology, al- 
though these may be the exciting causes acting upon a liver reduced in 
vitality. The influence of immoderate eating (especially of animal food), 
of drinking (especially alcohol), and of exposure to cold and fatigue may 
not be overlooked. These induce an active congestion of the liver, and 
on account of the consequent increased functional demands reduce its 
vitality, and perhaps in this way render the liver especially vulnerable to 
the deleterious influence of the causes of malaria, dysentery, etc. 

Pathology. — The lesions are most diverse; they include combinations 
of congestion, cloudy swelling, focal necroses, and the vascular and 
other phenomena of inflammation. The lesions vary from small focal 
necroses to more widespread, if not general, involvement of the liver. In 
slight or moderate cases the appearances of the liver are those of active 
45 



706 DISEASES OF THE LIVER 

congestion and cloudy swelling; in the more severe cases they vary in 
grade up to those of acute yellow atrophy. In some (protracted) cases, 
looked upon by many authors as a subacute form of acute yellow atrophy, 
there is more or less compensatory hyperplasia of the liver cells. 

Symptoms. — The symptoms virtually are those of active congestion of 
the liver, of which acute hepatitis is only an advanced stage. Perhaps, 
although not necessarily, the symptoms are more aggravated in the 
inflammatory than in the merely congestive disorder : the liver pain and 
tenderness are likely to be more marked; nausea and vomiting are more 
common and usually more severe; the vomited matter partakes of the 
so-called bilious character (greenish, watery), and not infrequently con- 
tains blood — due usually to violent and distressing retching that provokes 
marked thirst and ultimately may induce marked prostration or collapse; 
the bowels are likely to be constipated, but the constipation may alternate 
with a foul, ill-smelling diarrhoea; and the nervous symptoms, such as 
headache, restlessness, irritability, mental depression, disturbed sleep, 
etc., are usually more marked; slight jaundice may develop. The 
liver becomes enlarged — sometimes notably enlarged. In malarial cases 
the spleen also becomes enlarged. Fever (101° to 103° F.) supervenes 
and serves to distinguish the inflammatory from the merely congestive 
disorder. 

Diagnosis. — The diagnosis is usually apparent from the etiological fac- 
tors and the general symptoms. The diagnostic difficulties pertain to 
excluding other disorders, such as the different forms of suppurative 
hepatitis, and in the presence of jaundice, the different forms of toxic 
jaundice and acute yellow atrophy. In the early stages it is frequently 
quite impossible to differentiate between suppurative and non-suppu- 
rative hepatitis; in some cases time alone will bring the diagnosis. In 
some cases the one is a later stage of the other, and the suppuration may 
not be susceptible of recognition until the development of the general 
phenomena of the condition — irregular chills, fever, sweats, etc. In 
acute yellow atrophy the constitutional and nervous symptoms are more 
severe, the liver, at first enlarged, becomes small, the duration is less, and 
the outcome is usually death. 

Prognosis. — The first attack of acute non-suppurative hepatitis, espe- 
cially as observed in the tropics, usually lasts about a week or ten days, 
and results in recovery; in some cases, however, suppuration ensues. 
The one attack, however, predisposes to subsequent attacks, and with 
each recurrence the course and termination are less favorable. 

Treatment. — The treatment of acute non-suppurative hepatitis (as 
well as of its antecedent stage — active congestion) comprises the avoid- 
ance of all factors likely to produce it: therefore, wisdom and moderation 
in eating and drinking; in the tropics, prophylaxis of the infections 
known to involve the liver (malaria, dysentery, etc.). When the attack 
has developed, the patient should go to bed and be kept there until 
convalescence is complete. The guiding principle should be to reduce 
the functional demands upon the liver, to eliminate all factors that 



SUPPURATIVE HEPATITIS 707 

might provoke or add to its congestion, and to reduce any existing intes- 
tinal catarrh. These objects are best achieved by dietary regulations. 
The diet should be minimal in amount and absolutely unirritating; in 
general it should consist exclusively of milk, which should be given at 
stated (rather long) intervals, and well diluted with lime water, Vichy, 
or other alkaline water. Whey, junket, albumen- water, strained broths 
(without seasoning), barley water, calf's foot jelly, etc., may be given 
later. The bowels should be thoroughly evacuated, preferably by saline 
cathartics; later, by calomel or blue mass. Ammonium chloride (60 
grains, 4 grams, daily) is extensively used by physicians in the tropics, 
and is believed to control the congestion and prevent inflammation of 
the liver, to relieve the intestinal catarrh, and to promote the elimination 
(by diuresis) of retained waste products (urea, uric acid, etc.). It may 
be given in the early stages, when it should be combined with the alkalies 
(alkaline waters, sodium bicarbonate, etc.), or later, when it may be com- 
bined with nitrohydrochloric acid (highly extolled in hepatic torpidity), 
nux vomica, or strychnine, and a bitter tonic (gentian, columba, quassia, 
etc.). The distressing gastric irritability of the early stage of some cases 
may be controlled by sodium bicarbonate, bismuth subnitrate, and car- 
bolic acid or creosote. Intestinal antiseptics may be useful: /?-naphthol, 
bismuth, resorcin, salol, etc. These subject to exacerbations or recur- 
rences of acute congestion of the liver are much benefited by treatment 
at such spas as Carlsbad, Marienbad, Vichy, Ems, Saratoga, etc. 

Suppurative Hepatitis. — Suppurative hepatitis (abscess of the liver) 
occurs under a variety of circumstances and in several forms. There is 
some justification for the common division into two classes — the large, 
single, so-called tropical abscess, and the small, multiple, non- tropical 
abscesses; but the processes are not altogether different, since the tropical 
abscess may be double instead of single, and even when single, by in- 
fecting adjacent liver tissue, may give rise to the development of many 
secondary abscesses, and a number of small abscesses by peripheral 
extension may eventually coalesce and give rise to a large single abscess. 

Etiology. — Abscess of the liver is always the consequence of micro- 
organismal infection; the microorganisms are various, and they reach the 
liver by one of several pathways. The common causative microorganisms 
are the ordinary staphylococci and streptococci, Amoeba coli (Entamoeba 
dysenterise), Bacillus coli communis, Bacillus pyogenes foetidus, Bacillus 
typhosus, Bacillus dysenterise, Bacillus pyocyaneus, Diplococcus pneu- 
moniae, Proteus vulgaris, Actinomyces bovis, etc. The infecting agent 
or agents may reach the liver directly, as when, in consequence of trau- 
matism, bacteria are introduced directly into the liver, or when they 
reach the liver by extension of disease of adjacent organs; or the infection 
may be carried from afar by the blood stream, that is, by the portal vein 
(dysentery, and other causes of suppurative pylephlebitis); by the 
hepatic artery (general septicopyemic processes); by the hepatic veins 
(retrograde embolism); by the biliary ducts (suppurative cholangitis and 
pericholangitis); or by the lymphatics. 



708 DISEASES OF THE LIVER 

Pathology. — The liver is enlarged, swollen, and opaque, and presents 
the ordinary evidences of parenchymatous degeneration or cloudy swell- 
ing. In addition, in the cases of so-called multiple pyemic abscesses, it 
exhibits a number of variously sized abscesses — usually small, but often 
coalescing to form larger, sometimes many-chambered cavities, with puru- 
lent contents. The so-called single, tropical, or amoebic abscess of the 
liver is described by Manson as consisting at first of one or more grayish, 
ill-defined, anemic, circular patches, half to one inch or thereabouts in 
diameter, in which the lobular structure of the liver cannot be made out. 
A drop or two of reddish, gummy pus may be expressed from the necrotic 
patches. Later, the centre of these patches liquefy, and distinct but 
ragged abscess cavities are formed. An abscess thus commenced ex- 
tends partly by molecular breaking down; partly by more massive 
necrosis of portions of its wall; partly by the formation of additional 
foci of softening in the neighborhood and subsequent breaking down of 
the intervening septa. These may involve almost if not an entire lobe, 
usually the right. The pus is usually thick, viscid, chocolate-colored, and 
streaked with blood, and often contains large pieces of necrotic liver 
tissue. Entamoeba dysenterise may be found in more than one-half of 
the cases (in some of the other cases in the wall of the abscess). The 
ordinary pyogenic organisms are rarely encountered. A large abscess 
may consist of a suppurating hydatid cyst. 

Symptoms. — Multiple septicopyemic abscesses, whether due to portal- 
vein, hepatic-artery, hepatic-vein, or biliary-duct infection, are often not 
recognized, since the symptoms of the primary disorder overshadow 
those due to the infection of the liver. In some cases, however, the 
spread of the infection to the liver is suggested by aggravation of the 
general symptoms, especially chills (or chilliness), fever, sweats, and poly- 
nuclear leukocytosis, and the development of local symptoms referable 
to the liver. These consist of pain in the region of the liver, perhaps 
referred to the right shoulder, tenderness about the liver, a mild grade of 
jaundice, and enlargement of the liver. The enlargement may be 
nodular, and the nodules soft and perhaps semifluctuating, and audible 
and palpable frictions may be detected. 

The so-called tropical abscess of the liver, although, as a rule, more 
readily recognized, may be \evj indefinite in its clinical manifestations, 
and escape clinical detection. Generally, the onset is insidious: some- 
times for weeks or months the patient may complain of general ill health, 
malaise, or increasing weakness — which are especially significant if they 
constitute part of the poor health or delayed convalescence following 
dysentery or other intestinal suppuration or ulceration. In some cases 
the onset is sudden, attended by a chill. The important symptoms are 
those of general septicopyemia — chills, fever, sweats, and polynuclear 
leukocytosis, to which local signs referable to the liver are added. 
The fever may be quite high (104° to 105° F.), and distinctly inter- 
mittent in character. Jaundice occurs in about 16 per cent, of the cases, 
and the patient may develop a suggestive icteroid facial aspect. The 



CHRONIC INTERSTITIAL HEPATITIS 709 

liver becomes enlarged; in the early stages, when the abscess is still 
well within the substance of the organ, the enlargement may be tolerably 
uniform, but as the abscess increases in size, it commonly causes dispro- 
portionate enlargement upward, usually of the right lobe — which may 
assume a characteristic dome shape; that is, the upper limit of hepatic 
dulness rises near the mammillary line, reaches its highest point (fourth 
or third rib) near the midaxillary line, and descends, so that in the mid- 
scapular line it may be as low as the angle of the scapula. The z-rays 
may disclose the extent and development of the liver enlargement better 
than percussion. Nausea and vomiting may occur; diarrhoea is rather 
common, and the patient emaciates. Perforation may occur, especially 
upward through the diaphragm, the pleura, and the lungs, giving rise to 
a so-called hepatopulmonary abscess; the expectoration is quite charac- 
teristic and has been likened to anchovy sauce. Rupture may occur also 
into the gastro-intestinal tract, externally, etc. 

Diagnosis. — The diagnosis is often difficult; the most suggestive signs 
consist of one of the several etiological factors, pain in the region of the 
liver, progressive enlargement and tenderness of the liver, slight jaundice, 
and chills, fever, sweats, and polynuclear leukocytosis. Leukocytosis, 
however, may be absent in slow-growing, chronic, and well-encapsulated 
abscesses. Malaria may be excluded by a history of antecedent dysen- 
tery or other etiological factor; evening rise in temperature (that of 
malaria being more common during the day); disproportionate enlarge- 
ment of the liver as compared with the spleen (the reverse being the case 
in malaria); absence of malarial parasites in the blood; the occurrence of 
polynuclear leukocytosis; and the non-response to quinine. Cholelithiasis 
and Charcot's biliary intermittent fever may be excluded by the absence 
of a history of cholecystitis, cholelithiasis, and biliary infection; the 
absence of attacks of fever, etc., separated by longer or shorter periods 
of apyrexia; the non-occurrence of increase in the jaundice after each 
attack; and the absence of serious impairment of the general health 
despite the long duration of the disorder. 

Prognosis. — The septicopyemia, of which the multiple liver abscesses 
are merely a part, is almost invariably fatal. Many of the so-called 
single or tropical abscesses result in recovery after operation. 

Treatment. — The treatment of the multiple septicopyemia abscesses is 
that of septicopyemia in general, and is quite as ineffectual. Perhaps 
treatment by specific bacterins may yet prove of service. The treatment 
of the large, single abscess is surgical and consists of thorough evacua- 
tion and drainage. 

CHRONIC INTERSTITIAL HEPATITIS: THE CIRRHOSES OF THE 

LIVER. 

Eliminating from consideration cases of (1) so-called capsular cir- 
rhosis (more properly called perihepatitis or hepatic capsulitis), in which 
the liver tissue may be not at all affected, except perhaps secondarily in 



710 DISEASES OF THE LIVER 

consequence of compression or by slight ingrowth of new connective 
tissue from the capsule; (2) so-called cardiac cirrhosis or cardiac liver, 
which develops in consequence of long-standing passive congestion; (3) 
syphilis of the liver, in which the lesions are specific and peculiar to that 
infection; and (4) circumscribed or focal fibroses, which follow limited 
inflammatory and degenerative processes, focal necroses, chronic ob- 
struction of the biliary ducts (pericholangitis), etc. — there are two types 
of chronic diffuse disorder of the liver attended by fibrosis, to which the 
term cirrhosis may be limited. One of these disorders is very common; 
it is usually due to the misuse of alcohol, or perhaps other poison carried 
by the portal circulation; it is characterized by moderate enlargement 
of the liver (which in advanced stages may become reduced in size), by 
newgrowth of connective tissue, especially conspicuous in and about the 
portal spaces, by phenomena of portal obstruction (notably hematemesis 
and ascites), and by the absence or unimportance of jaundice; and after 
the development of symptoms it usually runs a comparatively short 
course (Laennec's, portal, alcoholic, atrophic, or multilobular cirrhosis). 
The second of these disorders is rare; it is of unknown etiology; it is 
characterized by marked and persistent enlargement of the liver and 
spleen, by chronic jaundice, by periodic attacks of abdominal pain and 
fever, and by the absence of manifestations of portal obstruction (notably 
ascites); the essential lesion is a radicular cholangitis, and it runs a com- 
paratively long course (Hanot's, biliary, hypertrophic, or monolobular 
cirrhosis. 

In conditions of long-standing obstruction to the large biliary ducts, 
especially from gallstones, more or less fibrosis develops in and about the 
smaller biliary ducts in the liver, and may spread to the adjacent liver 
tissue; the ensuing induration is sometimes spoken of as obstructive 
biliary cirrhosis (more properly cholangitis and pericholangitis). 



PORTAL CIRRHOSIS. 

Portal cirrhosis is a chronic degenerative and inflammatory disease of 
the liver characterized by recurring degeneration and regeneration of the 
hepatic parenchyma and by concomitant and consecutive fibrosis in and 
about the interlobular or portal spaces, all of which leads ultimately to 
obstruction of the portal circulation. 

Etiology. — Portal cirrhosis is most common during the fifth decade; 
although it is by no means rare at the extremes of life. A number of 
cases occur in young children, in whom it is often fatal before the sixth 
year. It is a little more than twice as common in men as in women. It 
is undoubtedly the expression of the activity of some poison or poisons; 
these are various in nature, and may reach the liver by way of the portal 
vein, the hepatic artery, or both. In the great majority of cases it follows 
addiction to alcohol, especially distilled liquors (whiskey, gin, brandy, 
etc.), which are a direct poison to the hepatic parenchyma, and set up 



PORTAL CIRRHOSIS 711 

also gastro-intestinal catarrh; this doubtless results in the formation of 
divers autotoxins that may injuriously affect the liver. A special form of 
cirrhosis; believed to be due to highly seasoned food, fermentative dys- 
pepsia, etc., is recognized (Budd's non-alcoholic or dyspeptic cirrhosis). 
Infections of various kinds, such as malaria, tuberculosis, syphilis, 
uncinariasis, distomatosis (bilharziosis), etc., may be followed by cir- 
rhosis, but the relationship of the one to the other has not been deter- 
mined; in most cases the necroses and fibroses are focal, and the lesions 
are not really cirrhotic in an acceptable sense. Cirrhosis is also asso- 
ciated with a type of hemolysis (hemochromatosis). 

Pathology. — The liver varies much in size in different cases, and in 
the same case at different times. At the necropsy it may be very small, 
weighing only 980 grams or less; or it may be very large, weighing as 
much as 4000 grams or more; but it is worthy of note that in the majority 
of cases at the necropsy it weighs more than normally. It is of 
increased density, increased consistency, and lessened elasticity. The 
capsule is often thickened 'and united to the diaphragm by adhesions. 
The surface of the organ is distinctly granular, the small livers more so 
than the larger ones: grayish-white depressions alternate with pale, 
yellowish-brown, sometimes reddish-brown, roundish or ovoid elevations 
— the so-called coarsely granular or " hobnail' ' liver. The cut surface of 
the liver reveals interlacing bands of whitish or grayish-white fibrous con- 
nective tissue that vary somewhat in thickness, pervade the entire organ, 
and are continuous with the grayish opaque depressions on the surface 
of the liver. These bands of fibrous connective tissue, which obviously 
take their origin in the periportal spaces, form a network that encloses or 
surrounds islets of liver tissue that vary in size from that of a pinpoint to 
others 1 cm. or more in diameter; the larger islets are made up of several, 
often eight, ten, or more liver lobules (or remains of liver lobules), and are 
pervaded by more delicate bands of connective tissue (so-called multi- 
lobular cirrhosis). The liver tissue is usually pale yellowish in color or 
yellowish brown (u'ppk, yellowish); occasionally it is greenish (from 
staining with bile), or reddish or brownish, especially in the centres of the 
lobules (from staining with blood or blood pigment). Microscopically, 
the essential lesions consist of a variable degree of destroyed, atrophic, 
hyperplastic, and rearranged hepatic parenchyma and of newgrown 
fibrous connective tissue. In consequence of the activity of some 
poison, larger or smaller areas of liver cells are destroyed. The sur- 
viving cells attempt by hyperplasia to compensate for the cells lost. 

The continuing activity of the etiological factor leads to a continuous 
or recrudescing death of certain old as well as newly formed liver cells, 
which in turn is followed by renewed regeneration. This continuous 
degeneration and regeneration ultimately lead to complete transforma- 
tion of the architecture of the liver, certain lobules are entirely destroyed, 
others are partly or completely rearranged, some are markedly hyper- 
plastic, although tolerably well arranged, some show dendritic and other 
irregular proliferation (including the newly formed, so-called, pseudo-bile 



712 DISEASES OF THE LIVER 

ducts), new islets of liver tissue entirely devoid of central veins appear, 
and, what is especially important, new circulatory conditions — capillary 
and venous — arise. In some cases there is considerable fatty infiltration 
of the liver cells (so-called fatty cirrhosis). 

Concurrent with the degeneration of the liver cells, the interstitial con- 
nective tissue early shows more or less round-cell infiltration and other 
inflammatory phenomena, especially in and about the portal spaces; 
later there is considerable increase in the amount of connective tissue — 
in part the result of organization of the inflammatory exudate, in part a 
replacement fibrosis to fill up potential lacunae left by destroyed liver 
parenchyma, in part the tissue originally between the lobules (the con- 
nective tissue of Glisson's capsule), and in part the collapsed and other- 
wise altered reticulum of certain liver lobules the cells of which have dis- 
appeared. This newly formed connective tissue commonly encloses 
rather than invades the liver lobules; sometimes only one lobule is en- 
closed in a wide band of connective tissue, sometimes many lobules — 
whence the designation multilobular cirrhosis. There is usually also 
considerable increase in the elastic tissue. This fibrosis ultimately con- 
tracts, and on the one hand causes atrophic changes in the liver cells, and 
on the other, obstruction and obliteration of some of the interlobular and 
intralobular branches of the portal vein. 

The spleen becomes enlarged in 80 per cent, of the cases — the conse- 
quence of toxic hyperplasia and of passive congestion. The gastro- 
intestinal tract becomes congested and chronically inflamed, and 
reveals many dilated and tortuous veins, which, rupturing, give rise to 
more or less severe hemorrhage. The kidneys may reveal chronic inter- 
stitial changes. The heart and the pancreas often become fibrosed. 
The peritoneum is commonly thickened, and not infrequently becomes 
the seat of miliary tuberculosis (which may determine the final lethal 
issue). 

Communications between the portal vein and the systemic circulation 
constitute a part of the cirrhotic process. For the most part these con- 
sist of dilatations of normally existing anastomoses. The important are 
(Rolleston): (1) A general anastomosis between the veins of the perito- 
neum and those of the abdominal wall, such as the lumbar and renal. 
(2) Those around or in connection with the liver, especially the para- 
umbilical veins (Sappey) of the falciform ligament, which put the portal 
vein in communication with the veins of the anterior abdominal wall. 
This anastomosis may show itself as a " caput medusas," or a number 
of dilated veins around the umbilicus. This must be distinguished from 
the more marked venous anastomoses which result from obstruction to 
the passage of blood along the inferior vena cava; in the latter the 
dilated epigastric and mammary veins avoid and do not centre around 
the umbilicus. (3) Between the oesophageal veins, discharging into the 
azygos veins and thence into the superior vena cava, on the one hand, 
and the gastric veins, on the other. These veins may become varicose 
(oesophageal varices or piles), and are a common cause of profuse and 



PORTAL CIRRHOSIS 713 

even fatal hemorrhage. (4) Between the superior hemorrhoidal veins, 
tributaries of the inferior mesenteric vein, and the middle and inferior 
hemorrhoidal veins which open into the internal iliac veins (the cause 
of piles). These anastomoses serve both a useful and an evil purpose. 
On the one hand, as long as the collateral circulation is efficient, obstruc- 
tive symptoms are in abeyance and the disordered liver is enabled better 
to perform its functions, perhaps enabled to regenerate, whence in some 
cases the disease remains or becomes latent, even apparently cured; on 
the other hand, (a) the dilated veins are likely to rupture, either spon- 
taneously or in consequence of trauma, and lead to more or less severe 
hemorrhage (hematemesis, enterorrhagia, hematoma of the abdominal 
wall about the round ligament); and (b) much of the blood from the 
gastro-intestinal tract being thus diverted from the liver to the general 
circulation, conditions somewhat analogous to those induced by the 
establishment of an Eck's fistula (the experimental communication 
between the inferior vena cava and the portal vein), supervene, much 
of the products of digestion is not brought under the influence of the 
liver, is not detoxified, and toxemia ensues. 

Symptoms. — Cirrhosis of the liver may remain for many years entirely 
latent; indeed, in most cases the lesions in the liver are well advanced 
before the onset of noteworthy symptoms, and the disease not infre- 
quently constitutes an unexpected finding at the necropsy table. Symp- 
tomatically, the disease has been divided into the preascitic and the 
ascitic stage, and the symptoms are described as being (1) obstructive, 
and (2) toxic. As long as the collateral circulation is efficient, obstructive 
symptoms are in abeyance. 

In a few cases, during the early stages of the development of the dis- 
ease, phenomena attributed to an ill-defined, so-called, active hyperemia 
of the liver are encountered; that is, the patient complains of ill-defined 
or vague gastric symptoms, a sense of weight in the right hypochon- 
drium, perhaps short transitory attacks of slight fever, slight jaundice, 
and actual pain in the region of the liver; and the liver on examination is 
ound to be enlarged and tender. Such attacks may last several days, 
disappear, and recur at longer or shorter intervals. 

In most cases, however, the early symptoms are an expression of 
gastro-intestinal catarrh — due partly to portal congestion, and partly, in 
many cases at least, to chronic alcoholism with acute exacerbations. 
The patient complains of coated tongue, irregular appetite, flatulence, 
epigastric distress, especially after eating, sometimes of nausea and vom- 
iting (often in the morning, and usually referable to alcoholism), irregular 
action of the bowels (alternating attacks of diarrhoea and constipation), 
or habitual constipation, hemorrhoids, etc. The increasing portal 
obstruction leads to increasing congestion of the gastro-intestinal tract 
and the spleen, the congestion being doubtless favored by the absence of 
valves in the portal tributaries. This congestion reduces the functional 
capacity of the stomach and intestines, limiting the digestive juices and 
the intestinal secretions (although sometimes increasing the mucus), 



714 DISEASES OF THE LIVER 

reducing the absorbing power of the intestines, and ,often inhibiting 
peristalsis. Constipation increases and tympanites not infrequently 
ensues, and both may become of high grade and distressing; occasional 
relief is sometimes afforded by attacks of diarrhoea which relieve the 
engorged vessels. These phenomena, while not diagnostic, are highly 
suggestive of the disease, especially in association with a history of alco- 
holism. 

With the progress of the disease the foregoing evidences of derangement 
of the gastro-intestinal tract become more marked, and the general health 
becomes impaired; but the first obtrusive manifestation of the disease, 
that which induces the patient to seek medical advice, is not infrequently 
hematemesis or ascites. 

Hematemesis is an initial symptom in some cases, and it is a common 
event some time in the course of most cases. Usually it occurs early — 
while the liver is large; when not the initial symptom, it is often the first 
evidence of serious disease (33 per cent, of the cases); but it may occur 
late in the disease, that is, after the development of ascites and when the 
liver may have become small. With the hematemesis there is usually 
blood in the stools; but blood may occur in the stools without the vom- 
iting of blood, especially when the bleeding into the stomach is slow, and 
also when, as is not uncommon, the source of the blood is the intestine 
or the rectum or hemorrhoids. In suspected cases of cirrhosis exami- 
nation of the stools for blood (even occult blood) should be early resorted 
to. Hemorrhage from or into other parts of the body is very common, 
especially epistaxis, bleeding from the gums, larynx, lungs, and into the 
skin and mucous membranes. 

Jaundice is not a part of portal cirrhosis, but it occurs as a complication 
some time during the course of from 15 to 20 per cent, of the cases, and is 
usually due to radicular cholangitis. 

Toxic symptoms may develop at any time during the course of the dis- 
ease. Minor symptoms consist of restlessness, weakness, headache, and 
itching; the itching may precede or be unassociated with jaundice. 
More severe toxic symptoms comprise: (1) Apathy, stupor, and coma; 
(2) an active noisy delirium; and (3) convulsions, paralyses, contrac- 
tures, one of which may alternate with the others. 

Cirrhosis of the liver may be afebrile throughout its course; during the 
terminal stage the temperature maybe subnormal; but attacks of fever 
(100° to 102.5° F.) are not uncommon. Sometimes these seem to be part 
of the disease, especially when it advances rapidly; sometimes they are 
due to attacks of perihepatitis; sometimes they are due to complications. 
The more continuous fever, which is rather common late in the disease, is 
usually due to tuberculosis — of the peritoneum, lungs, etc. 

Physical Signs. — The abdomen is more or less markedly, sometimes 
enormously, distended, and is in notable contrast to the emaciated, sub- 
icteroid face and extremities. The abdominal wall reveals enlarged and 
varicose veins due to the collateral circulation. The liver is enlarged 
in most cases, but the size varies considerably in different cases and in the 



PORTAL CIRRHOSIS 715 

same case at different times. Its surface may be distinctly rough to pal- 
pation ("hobnails"). In some cases late in the course of the disease the 
liver becomes considerably reduced in size. The spleen is usually en- 
larged, palpable two or three fingers' breadth below the left costal margin. 
It is often much reduced in size by copious gastro-intestinal hemorrhage, 
severe diarrhoea, the recurrence of ascites after tapping, etc. 

Ascites is often the first obtrusive manifestation that leads the patient 
to seek medical advice. It is usually a late event. In most cases the 
liver is larger than normally at the time of development of the ascites; 
but a large liver may be present without ascites; a small liver is rarely 
found without ascites. The fluid varies in amount — in the average case 
from 4 to 8 or 10 liters, but it may be as much as 20 liters. It is due to 
different causes: (1) Portal obstruction, the result of lessening of the 
portal area in the liver, and the communication of the hepatic-artery 
pressure to the portal- vein radicles; (2) a complicating perihepatitis or 
more widespread peritonitis, which is very corhmon in the late stages of 
the disease; and (3) toxemia; the toxic agent is not known, but it is 
believed to act as a lymphagogue on the peritoneum. Varying with the 
amount of fluid, there is more or less displacement and compression of 
the abdominal and thoracic organs. The liver and the diaphragm are 
pushed upward and cause embarrassment of the respiration and the 
heart action, and not infrequently compression and consequent con- 
gestion and collapse, and perhaps bronchopneumonia, of the bases of 
lungs, particularly the right. (Edema is common late in the disease, 
occasionally it may precede the ascites, in which event it is toxic, anemic, 
cardiac, or renal in origin. The blood shows the changes of secondary 
anemia. There is no leukocytosis unless there is some associated infec- 
tion, which is not rare. Late in the disease evidences of considerable 
toxic disorganization of the blood become apparent — hydremia, oedema, 
submucous and subcutaneous hemorrhages, etc., and the blood findings 
rarely may simulate those of pernicious anemia. 

Complications. — Infections of various kinds are common, especially 
tuberculosis — of the lungs, pleura, or peritoneum. Tuberculous perito- 
nitis is very common, and not infrequently determines the fatal issue. 
It is suggested by fever, tenderness and rigidity of the abdominal wall, 
perhaps increase in the amount of ascites previously stationary (the 
fluid may become hemorrhagic), more rapid course, and speedy death. 
Chronic nephritis occurs in about one-half of the cases. 

Diagnosis. — The diagnosis of cirrhosis of the liver in the early stages is 
not always an easy matter, but it should be made more frequently than 
it is. In an alcoholic subject with dyspepsia, an enlarged and tender liver 
suggests the diagnosis; and this is virtually confirmed if to these there be 
added an enlarged spleen, perhaps recurring attacks of pain in the region 
of the liver, with slight fever or slight jaundice, and urobilinuria. Later, 
when hematemesis, ascites, the hepatic facies, etc., have developed, the 
diagnosis can be no longer in doubt. When the liver is enlarged and there 
is no ascites, one must exclude other causes of enlargement of the liver, 



716 DISEASES OF THE LIVER 

such as passive congestion, fatty liver, amyloid liver, leukemia, malaria, 
and syphilis. The occurrence of hematemesis and other gastro-intestinal 
hemorrhages necessitates differentiation from gastric and duodenal ulcer. 
When ascites has developed, one must exclude other causes of ascites, 
such as chronic peritonitis and perihepatitis (multiple serositis), throm- 
bosis of the portal vein, tumors of the peritoneum and abdominal organs, 
chronic cardiac disease, and cachectic states. Splenic anemia (Band's 
disease) also must be considered in some cases. 

There are several special types of portal cirrhosis, of which the fol- 
lowing are the most important: (1) Hemochromatosis (bronzed dia- 
betes), a disorder that occurs especially in male adults, and is characterized 
by pigmentation of the viscera and usually also of the skin; cirrhosis of 
the liver; and fibrosis of the pancreas, with involvement of the islands 
of Langerhans and consequent diabetes. The pigmentation is usually 
attributed to increased hemolysis. The noteworthy symptoms consist 
of general cutaneous pigmentation (suggesting Addison's disease), 
enlargement of the liver and spleen, and the ultimate development of 
diabetes. Ascites may be slight or absent; hemorrhages may or may 
not occur, but death may result from rupture of oesophageal varices. 
Diabetes, when it supervenes, is severe and dominates the clinical phe- 
nomena; acidosis is common and usually leads to coma. (2) Malarial 
cirrhosis is said by those of experience to occur in the tropics. (3) 
Anthracotic cirrhosis is very rare. (4) Cirrhosis in children is usually of 
the portal type. The symptoms in general conform to those in the adult. 
Hematemesis is less common (greater distensibility of the spleen in chil- 
dren), diarrhoea and slight jaundice are more common; the liver and the 
spleen are disproportionately larger than in adults (relatively greater 
volume and more ability for repair in children); tuberculous peritonitis 
is common, and perhaps accounts for most of the ascites and the not 
uncommon fever. 

Prognosis. — The prognosis is not encouraging. Ordinarily the disease 
runs a fatal course within three years from the onset of symptoms. 
Doubtless if the disease were earlier recognized, arrest could be secured 
in many cases. 

Treatment. — The only trustworthy treatment is based upon our con- 
ception of the etiological factors, and consists essentially in the avoidance 
of all causes known or suspected to lead to the disease. Of these, the 
most important are alcohol, stimulating and highly seasoned foods, foods 
likely to undergo fermentation in the intestinal tract, etc., all of which 
must be strictly prohibited. Milk is the best diet for a month or six 
weeks, and from time to time alkaline waters may be added to it. Later, 
one may give also eggs, gruels, cereals, stewed fruits, fish, and green 
vegetables, and some meat from time to time. Good results sometimes 
follow the prolonged use of the iodides, to which minute doses of mercuric 
bichloride may be added. Nitrohydrochloric acid and ammonium 
chloride are said to be efficacious in some cases. Indigestion, nausea, 
vomiting, hematemesis, constipation, diarrhoea, etc., are to be treated 



BILIARY CIRRHOSIS 717 

as mentioned under those headings The ascites, if not relieved by 
purgatives (blue mass or calomel and saline cathartics), diuretics (alka- 
line diuretics, theobromine, spartein, caffeine, apocynum cannabinum), 
the Niemeyer pill (page 477), and a dry diet, should be tapped. The 
Talma -Morrison operation (omentopexy, epiplopexy) is of service in 
carefully selected cases early. It is designed to relieve the portal circu- 
lation, by diverting the portal blood to the general systemic circulation 
through the medium of adhesions set up between the liver, the omentum, 
and the parietal peritoneum. Associated cardiac, pulmonary, or renal 
disease, repeated tappings, jaundice, toxemia, and emaciation are 
contra-indications to performing operation. 



BILIARY CIRRHOSIS. 

Biliary cirrhosis is a chronic disorder of the liver, probably infectious 
in origin, characterized anatomically by radicular cholangitis and con- 
nective-tissue hyperplasia, and clinically by chronic jaundice and enlarge- 
ment of the liver and spleen. 

Etiology. — Biliary cirrhosis is especially common during adolescence 
and early adult life; most cases occur between the twentieth and the 
thirtieth year; it is rare after the fortieth year, but it is quite common in 
children (juvenile type), especially in India. In adults about 85 per 
cent, of the cases occur in males; in children it is equally common in 
the two sexes. A seeming hereditary influence is not uncommon. 

The exact nature of the disease is not known. Some, but not all, sub- 
jects are alcoholic; and, on the whole, it seems that alcohol plays at most 
a minor etiological role. In the cases so common in children in India 
it is not in any way an etiological factor. In other cases, perhaps, it 
reduces the resisting power of the liver and thus permits of the more 
ready operation of other causes. There is some inconclusive evidence 
that the disorder is the consequence of a general blood infection that 
provokes a radicular cholangitis; but no definite etiological agent has 
been discovered. An infection is suggested by the disorder sometimes 
developing after infectious diseases, by the common occurrence of attacks 
of fever and leukocytosis, and the not rare occurrence of general lymph- 
node enlargement. 

Pathology. — The liver is enlarged and weighs from 2000 to 4000 grams; 
its shape is maintained, its consistency increased, and its elasticity dimin- 
ished. The surface is smooth and exhibits very fine granulations (in 
marked contrast to the coarse granulations of portal cirrhosis). The 
liver is usually dark olive green in color. The cut surface is dark greenish 
or yellowish green in color, smooth, or very slightly granular in advanced 
cases; usually the liver lobules are more or less obvious, sometimes 
apparently enlarged, and always separated by widened trabecule of 
connective tissue. Microscopically, the obtrusive feature consists of an 
overgrowth of fibrous connective tissue, which occurs in delicate fibrillar 



718 DISEASES OF THE LIVER 

bands that not only course between the lobules, but also invade the 
lobules to a greater or less extent (so-called monolobular, unilobular, 
or intralobular cirrhosis). In some advanced cases this arrange- 
ment of connective tissue is not so regular. The basic and essential 
lesion of the disorder, however, seems to be a radicular cholangitis — 
which is disclosed by proliferation and desquamation of the epithelium 
of the small biliary ducts. This leads to obstruction and consequent 
dilatation of the biliary canaliculi, which in turn are found distended with 
inspissated bile and bile thrombi. Branching columns of cells, so- 
called pseudobiliary canaliculi, in and about the periphery of the liver 
lobules (due to hyperplasia of the liver cells as well as of preexisting 
ducts), constitute a noteworthy feature of the lesions. The liver cells 
exhibit rather inconspicuous lesions, but acute necrotic autolytic changes 
may occur at any time and determine the fatal issue. All the organs of 
the body are bile-stained. The spleen is enlarged, and commonly 
weighs 600 to 1500 grams or more; in children it may be as large as, if 
not larger than, the liver. The lymph nodes in the portal fissure are 
enlarged, cedematous, and congested, but they exert no pressure on the 
biliary ducts. Occasionally the lymph nodes in other parts of the body 
are similarly, although less, affected. 

Symptoms. — The onset of the disease is insidious; for a long time there 
may be ill-defined complaint of poor health, general malaise, weakness, 
loss of flesh, etc.; or there maybe a sense of weight or distress, perhaps 
actual pain, in the right hypochondrium; rarely there is some dyspepsia, 
coated tongue, poor appetite, perhaps nausea, diarrhoea, etc.; in a few 
cases the patient's attention may be first directed to increase in the size 
of the abdomen. 

In the great majority of cases the first obtrusive symptom is jaundice. 
This varies in degree from time to time, periods of exacerbation and of 
regression alternating; but, on the whole, it tends to increase with the 
progress of the disease, and eventually it may become extreme, usually 
greenish. The usual concomitants of protracted jaundice are seen; 
there is often intense itching, eczema, lichen, sometimes xanthelasma, 
etc.; bleeding from the nose or the gums or other mucous membranes 
may occur from time to time for a long period, or there may be recurring 
attacks of purpura; the urine shows the presence of bile pigment. The 
feces also contain bile pigments and may be very dark (in contrast to the 
clay- colored stools of obstructive jaundice). 

In addition, the disease is characterized by periodic attacks of more 
or less severe abdominal pain, especially in the region of the liver, some- 
times attended by nausea and vomiting, and associated with fever, 
leukocytosis, and increase of the jaundice. These attacks occur without 
regularity and without demonstrable cause, and they last variable periods 
— several days to several weeks. Usually the fever does not go above 
102°; in some cases there is slight fever for long periods. Occasionally 
these exacerbations are attended by the nervous and other phenomena of 
icterus gravis, and with high fever, delirium, coma, etc., the patient may die. 



TUMORS OF THE LIVER 719 

Examination reveals the liver to be uniformly enlarged, reaching some- 
times to or below the transumbilical line; it presents a smooth or finely 
granular surface. The spleen also is enlarged, much more so than in 
portal cirrhosis. It is said that the enlargement of the spleen sometimes 
antedates that of the liver. In children the spleen may be actually larger 
and heavier than the liver — the juvenile type of biliary cirrhosis (cirrhose 
biliaire splenomegalique of Gilbert and Fournier). The blood reveals 
oligocythemia, leukocytosis (increased at the time of the periodic exacer- 
bations), and diminished coagulability. 

Rarely, a bulbous enlargement involving the soft tissues of the fingers 
and toes (Hippocratic fingers) occurs. In children, growth is stunted, 
a type of infantilism develops, and the onset of puberty is delayed. 

Diagnosis. — The important diagnostic features consist of the occur- 
rence in a young, usually non-alcoholic subject of chronic progressive 
jaundice, with considerable and persistent enlargement of the liver and 
spleen, and periodic attacks of abdominal pain, fever, and leukocytosis, 
with subsequent increase in the jaundice, and no sign of cholelithiasis 
or portal obstruction. There should be no difficulty in differentiating 
the more common or portal cirrhosis — which occurs, as a rule, in older 
and alcoholic subjects and is attended by more marked dyspeptic symp- 
toms and by evidences of portal obstruction (dilatation of the subcu- 
taneous veins of the abdomen and ascites), which are absent in biliary 
cirrhosis. In portal cirrhosis, hemorrhages, especially hematemesis, 
often occur early and are commonly profuse; whereas in biliary cirrhosis 
hemorrhages are usually a late manifestation and small. Jaundice 
sometimes occurs in portal cirrhosis, but it is a complication and catarrhal 
in nature; in biliary cirrhosis it is the conspicuous feature, and, although 
permanent, it is not associated with absence of bile from the feces. 
Portal cirrhosis usually runs a fatal course within three years or less; 
biliary cirrhosis not uncommonly lasts from five to ten years or more. 

Prognosis. — The outlook as regards cure is hopeless, but the disease 
may last for many years and the general health may be well maintained. 

Treatment. — The treatment is largely symptomatic. The hygienic 
conditions should be the best obtainable. The diet should be generous, 
but dietetic indiscretions, alcohol, etc., should be avoided. The prob- 
able infectious nature of the disorder has suggested the use of antiseptics, 
such as the salicylates and hexamethylenamin, which are eliminated 
with the bile; apparent improvement has been reported in some cases. 
Good results are said also to have followed drainage of the gall-bladder 
and the biliary ducts, but the diagnoses in some of these cases is open to 
question. 

TUMORS OF THE LIVER. 

Etiology. — Carcinoma of the liver may be primary or secondary (to 
carcinoma of the stomach, pancreas, intestine, rectum, female genitalia, 
breast, etc.). A primary growth is^[very rare,^the secondary being 



720 DISEASES OF THE LIVER 

from twenty-five to forty times as common. Both occur in adult life 
and old age. The primary tumor seems to be slightly more common in 
men than in women, the secondary slightly more common in women. 
Sarcoma and so-called benign growths are rare. 

Pathology. — Primary carcinoma appears under three forms: (1) Nod- 
ular or multiple carcinoma (65 per cent, of the cases) — numerous grayish- 
white nodules scattered throughout the liver; (2) massive carcinoma (23 
per cent, of the cases) — a large mass occupying almost, if not quite, an 
entire lobe; and (3) infiltrating or diffuse carcinoma (12 per cent, of the 
cases) — so-called cirrhosis with multiple adenoma or carcinoma. The 
growth may develop from the hepatic cells or the biliary epithelium. In 
some cases the sequence of events is represented by hepatic-cell hyper- 
plasia, adenoma, carcinoma. Secondary carcinoma appears as multiple 
grayish nodules scattered throughout the organ; these often become 
necrotic, softened, and umbilicated. Primary sarcoma may occur as a 
nodular or a diffuse growth; secondary sarcoma is usually melanotic in 
type, and follows a primary growth in the choroid coat of the eye. 

Symptoms. — The symptoms do not differ notably whether the growth be 
primary or secondary, and carcinomatous or sarcomatous. Usually the 
onset is insidious; the patient may complain of general ill health, languor, 
anemia, emaciation, etc., for a long time before the true nature of the 
disorder is disclosed; in many cases, certainly in at least one-third of the 
cases of secondary carcinoma, the actual conditions are recognized only 
at autopsy. In some cases, symptoms referable to the primary growth 
precede, for a variable time, symptoms significant of involvement of the 
liver; but in a considerable number of cases, carcinoma of the stomach, 
rectum, etc., may be for a long time latent, or the symptoms are not 
obtrusive, and the first noteworthy manifestations may be referable to 
the liver. In a small percentage of cases the primary growth remains 
insignificant; the lesions are most marked in the liver, and the symptoms 
almost, if not exclusively, hepatic. They consist of local pain and dis- 
tress, jaundice, ascites, and enlargement of the liver. The local discom- 
fort (or sense of weight) is usually proportionate to the size and rapidity of 
growth of the carcinoma; in some large carcinomas, however, there may 
be no actual pain. Jaundice occurs in more than one-half of the cases; 
it varies in degree at first, but tends to increase and to become perma- 
nent. If a large duct becomes obstructed, the stools become more or less 
pale, perhaps even clay-colored. Progressive enlargement of the liver is 
the phenomenon that determines the diagnosis. The enlargement may 
be moderate or great; it usually involves especially the right lobe, and 
it is characteristically nodular — the nodules often becoming umbilicated 
(softening, necrosis, or hemorrhage). Ascites occurs in about 20 per 
cent, of the cases, being due to portal obstruction or perihepatitis. 

In the course of time secondary nodules may develop along the falci- 
form ligament and become palpable through the linea alba or at the 
umbilicus, or in consequence of penetration of a branch of the hepatic 
vein, more distant metastases may supervene (lungs, etc.); the patient 



CONGENITAL OBLITERATION OF THE BILIARY DUCTS 721 

loses strength, and becomes anemic, emaciated, and cachectic; and phe- 
nomena attributable to hepatic insufficiency (cholemia) may develop. 

Diagnosis. — The diagnosis is not always possible, especially in the cases 
of secondary growths in which the deposits are few in number, small in 
size, and deep within the substance of the liver. In cases in which a 
primary growth is obvious or found on examination, and in which 
there is persisting severe jaundice, emaciation, cachexia, and a rapidly 
enlarging and nodular liver, the diagnosis can often be made on inspec- 
tion alone, especially if the patient be made to take a deep inspiration 
(whereupon the irregular nodular liver, covered only by a thin layer of 
skin, will be seen to descend). In the differential diagnosis one must 
exclude tumors of adjacent organs, as well as other causes of enlarge- 
ment of the liver, especially cirrhosis, syphilis, abscess, and hydatid 
disease. 

Prognosis, — The outlook is hopeless. The average duration of life 
after the development of symptoms referable to the liver is seven months. 

Treatment. — The treatment is purely palliative and symptomatic. 



DISEASES OF THE GALL-BLADDER AND 
BILIARY DUCTS. 

CONGENITAL OBLITERATION OF THE BILIARY DUCTS. 

Congenital obliteration of the biliary ducts is a disorder characterized 
anatomically by obliteration or atresia of the biliary ducts and biliary 
cirrhosis of the liver, and clinically by persistent jaundice and so-called 
cholemia, which proceed to a fatal issue. The nature of the disorder has 
not been definitely determined, at least for all cases. It may be the con- 
sequence of an anomaly of development, or it may be due to syphilis, to 
foetal peritonitis and adhesions, or to a form of hepatic cirrhosis with 
descending and obliterative cholangitis. Clinically, the disorder is char- 
acterized by jaundice, which is present at or develops soon after birth, 
although rarely it may be delayed for several months; it becomes per- 
sistent and intense. The stools become acholic, if not acholic from 
birth; the urine contains bile pigments; the liver and the spleen are 
enlarged; vomiting often ensues; and hemorrhages occur from the 
umbilical cord and into the subcutaneous and the submucous tissues. 
Gradually the infant emaciates; stupor, coma, or convulsions (cholemia) 
develop, and death ensues. The course of the disorder is rarely less than 
a week; usually it lasts for several weeks or several months. The more 
benign icterus neonatorum may be distinguished usually by the presence 
of bile in the feces and by the less marked jaundice which soon fades. 
Syphilis may be excluded by the absence of a history of syphilis in a 
parent, the absence of other evidences of syphilis, and the non-response 
to antisyphilitic treatment. 
46 



722 DISEASES OF THE GALL-BLADDER AND BILIARY DUCTS 

ACUTE CATARRHAL CHOLANGITIS. 

(Catarrhal Jaundice.) 

Etiology. — Acute catarrhal cholangitis is a common disorder in young, 
especially male, adults, although it occurs at all ages. It is usually due 
to dietetic indiscretions, such as eating too much food, or indigestible 
or tainted food, or overindulgence in alcohol — which set up a duodenal 
catarrh, which spreads to the biliary papilla and causes swelling of the 
mucosa and obstruction to the free flow of bile. Similar conditions 
sometimes occur in infections like pneumonia, typhoid fever, etc., in passive 
congestion of the duodenum, etc. Epidemics are sometimes observed. 

Pathology. — The lesions consist of congestion, swelling, oedema, and 
increased production of mucus at the lower end of the common bile duct 
and of the duodenal mucosa adjacent to the diverticulum of Vater. In 
some cases the swelling itself is sufficient to obstruct the flow of bile, but 
in other cases a plug of inspissated tenacious mucus effectually blocks 
the diverticulum of Vater. Eppinger found hyperplasia of the lymphoid 
tissue of the mucosa of that part of the common biliary duct that runs in 
the wall of the intestine; this had led to complete occlusion of the com- 
mon duct and dilatation of the rest of the biliary system. 

Symptoms. — In most cases the early symptoms are those of the pro- 
voking gastro-intestinal catarrh; loss of appetite, bad taste in the mouth, 
coated tongue, foul breath, epigastric distress, especially after eating, 
flatulence, nausea, and perhaps vomiting; there may-be constipation, or 
perhaps diarrhoea from extension of the intestinal catarrh; and the patient 
complains of headache, vertigo, mental depression, general malaise, etc. 
Rarely there is an acute onset, jaundice being the first symptom noticed; 
but in most cases after the mentioned symptoms have lasted for a few 
days to a week, the patient notices, or his attention is directed to the fact, 
that he is slightly jaundiced. The jaundice is of slow and insidious onset, 
and gradually increases. With the appearance of the jaundice, some- 
times before there is any obvious jaundice, the stools become pale in 
color and soon are devoid of bile pigment; the urine becomes scanty, 
dark in color, deposits an abundant sediment, and shows the presence of 
bile pigments. Usually the bile pigments can be detected in the urine 
before the appearance of the jaundice in the sclerotics. Pruritus is 
often marked; sometimes it even precedes the development of the jaun- 
dice. The itching is sometimes so extreme as to induce severe eczema, 
in consequence of uncontrollable scratching. The pulse usually is 
slowed, '60 or less per minute, and may reveal the dicrotism of low 
vascular tension. 

In most cases neither the liver nor the gall-bladder is palpably enlarged 
or tender. Fever (101°) is occasionally present, but it is rarely due 
directly to the cholangitis, except in the epidemic infectious cases; that 
which sometimes occurs at the beginning of the attack and lasts a day or 
two is probably due to the gastro-enteritis ; when conspicuous or when 



ACUTE CATARRHAL CHOLANGITIS ■ 723 

it lasts more than several days, it suggests some one of the types of toxic 
or infectious jaundice (of which, in reality, it may be a mild manifes- 
tation). 

At the end of about a week, sometimes not until later, the evidences of 
gastro-intestinal irritation subside; gradually the evidences of biliary 
obstruction lessen, bile pigments appear in the feces, and disappear, first 
from the urine and then from the skin, where, however, traces may be 
found for several months. Restoration of the general health is often 
much delayed; although the appetite may return at the end of a week 
or two, improvement in the general health does not occur until the bile 
pigments begin to be removed from the tissues. 

Diagnosis. — In most cases the diagnosis is readily made from the youth 
of the patient, an antecedent gastro-intestinal catarrh provoked by some 
more or less obvious cause, and the absence of local pain and of serious 
involvement of the general health (emaciation, etc.); the diagnosis is 
further confirmed by the benign and favorable course of the disorder, 
which in many cases definitely determines the diagnosis. Doubt re- 
garding its catarrhal nature should always be awakened by the occur- 
rence of jaundice in a middle-aged or elderly person, if it becomes deep 
or olive- tinted, and if it lasts more than six weeks; this is much more 
likely to be due to impaction of a gallstone or to carcinoma compressing 
the common duct. 

Prognosis. — As a rule, the prognosis is good; the disease of itself does 
not endanger life, and recovery is usually complete and lasting at the end 
of three to four or six weeks. 

Treatment. — The treatment is essentially that of the gastro-intestinal 
catarrh, commonly provocative of the cholangitis. The diet should be 
reduced and for several days should consist of a moderate amount of 
milk, preferably skimmed milk, or broth. The natural alkaline waters 
are serviceable; but alkalies, especially sodium bicarbonate, may be 
added to ordinary water. The bowels should be opened freely. Custom 
sanctions the use of calomel, which may be given in a single large dose or 
in repeated small doses (a blue pill is equally efficacious); it should be 
followed by a saline aperient. They should be given in sufficient dose to 
cause one or two free evacuations daily; more are undesirable. Injec- 
tions into the rectum of cold water are sometimes very efficacious in 
stimulating intestinal, and perhaps also gall-bladder, peristalsis. As the 
biliary stasis begins to subside, dilute nitrohydrochloric acid and bitter 
tonics render excellent service. Excessive flatulence is sometimes dis- 
tressing; it may be relieved by the use of bismuth salicylate, soda-mint, 
aromatic spirit of ammonia, chloroform water, and antifermentatives ; 
magnesia or rhubarb with sodium bicarbonate and charcoal also are of 
much service, and relieve the constipation. The pruritus may be relieved 
by cold sponging, or a carbolic-acid lotion (1 to 40), or the internal use of 
the bromides. 



724 DISEASES OF THE GALL-BLADDER AND BILIARY DUCTS 



SUPPURATIVE CHOLANGITIS. 

Etiology. — Suppurative cholangitis results from virulent bacterial infec- 
tion of the biliary ducts. The common infectious agents are Bacillus coli 
communis, staphylococci, streptococci, pneumococci, Bacillus typhosus, 
Bacillus aerogenes capsulatus, etc. The infection may occur by way of 
the portal or the general systemic circulation (descending infection), or 
by way of the duodenum and the diverticulum of Vater (ascending 
infection). In the great majority of cases there is some local disease of 
the biliary tract, which acts as an almost necessary predisposing factor; 
this comprises all disorders that interfere with the free circulation of the 
bile (that is, cause stagnation), and reduce the resistance of the biliary 
ducts, especially gallstones and tumors obstructing the duct. Usually 
there is associated disease of the gall-bladder. 

Pathology. — The biliary ducts are dilated, congested, cedematous, and 
filled with purulent material, usually bile-stained; and about the terminal 
branches of the biliary ducts within the liver there are few or many, small 
or moderately sized, abscesses. The liver tissue is the seat of cloudy 
swelling and more or less necrosis. 

Symptoms. — Usually there is a history of antecedent cholelithiasis or 
vague symptoms that may be interpreted as due to gallstones; in other 
cases there is some impairment of the general health, which, in the light 
of subsequent events, may be ascribed to malignant disease; in still other 
cases the patient suffers from, or has recently suffered from, some general 
infection, such as typhoid fever, pneumonia, etc. The onset is often 
insidious; occasionally the first noteworthy symptom is slight jaundice, 
but in perhaps most cases, especially in cases in which there has been 
antecedent jaundice due to other causes, the onset of the disease is an- 
nounced by constitutional phenomena, such as chills, fever, and sweats. 
These are usually severe, more or less frequently repeated at irregular 
intervals, and soon lead to considerable impairment of the general 
nutrition, emaciation, loss of appetite, nausea, perhaps vomiting, diar- 
rhoea, etc.; variable afebrile periods, however, are not uncommon. 
Jaundice is almost always present, but it is variable in degree; usually 
it is slight or moderate only, except in cases in which the cholangitis is 
associated with other conditions that cause intense jaundice. There 
may be dull aching or discomfort in the region of the liver (tension of 
the liver capsule); now and then there is more severe pain due to acute 
cholecystitis, cholelithiasis, obstruction of the ducts by tumors or worms, 
perihepatitis, peritonitis, etc. The liver is enlarged and usually con- 
tinues to enlarge under observation. Usually the gall-bladder also is 
enlarged and tender (acute cholecystitis). The spleen may be enlarged. 
Examination of the blood reveals polynuclear leukocytosis, more marked 
during and just after the febrile periods; sometimes it is absent during 
the afebrile periods. 



CHRONIC CATARRHAL CHOLANGITIS 725 

Diagnosis. — The diagnosis is usually apparent from a history of ante- 
cedent gallstones or other disorder of the biliary tract, or of typhoid fever 
or other infection, and the development of chills, fever, sweats, jaundice, 
local pain, progressive enlargement of the liver, perhaps also of the 
gall-bladder and spleen, and leukocytosis. 

Prognosis. — The prognosis is bad, but may be improved by thorough 
drainage of the gall-bladder and ducts undertaken early. 

Treatment. — Attempts should be made to prevent the disorder by 
thorough and efficient treatment of all forms and grades of biliary infec- 
tion (including gallstones). When suppurative cholangitis has devel- 
oped, the treatment is essentially surgical, and consists of the establish- 
ment of free drainage. The only available medical treatment comprises 
the use of antiseptics, such as the salicylates, hexamethylenamin, and 
other remedies, to disinfect the biliary tract and promote the free flow of 
bile. 

CHRONIC CATARRHAL CHOLANGITIS. 

Etiology. — Chronic catarrhal cholangitis may result from repeated 
attacks of acute catarrh, or from a low grade chronic infection. Usually 
it is found in association with gallstones; but it may be found also in 
chronic duodenal catarrh, and in obstruction due to tumors or strictures 
of the ducts. 

Pathology. — The lesions of chronic catarrhal cholangitis (of the larger 
ducts) consist of congestion and swelling of the mucosa, increased pro- 
duction of mucus, round-cell infiltration, and proliferation of the sub- 
mucosa and muscularis, with the production of new fibrous connective 
tissue; these lead to thickening and induration of the walls of the ducts 
and to pericholangitis. There may be partial or complete obstruction 
of the ducts. In the event of complete obstruction, the ducts become 
enormously dilated (up to the size of a thumb or larger); the gall- 
bladder and some of the intrahepatic ducts also become dilated. The 
contents of the biliary tract is usually a clear, almost colorless, often 
sterile mucus; when the mucus is sterile, the mucosa of the biliary tract 
is usually quite smooth. In the event of incomplete obstruction, the 
ducts, and especially the gall-bladder, are less dilated, the contents 
are usually turbid and often contain bacteria, and the mucosa may be 
more or less ulcerated. 

Symptoms. — The symptoms are those of chronic relapsing jaundice. 
Rarely, this may represent a direct continuation of an acute catarrhal 
jaundice, being more insidious in onset, and subject to exacerbations and 
remissions. The attending phenomena are those of acute catarrhal 
cholangitis — prolonged. In the cases of complete obstruction, the con- 
tents of the biliary tract being sterile, there is usually no fever, and 
remissions in the jaundice are slight. In the cases of incomplete ob- 
struction, remissions in the jaundice are more marked, and the contents 
of the biliary tract being infected, attacks of chill, fever, and sweats are 



726 DISEASES OF THE GALL-BLADDER AND BILIARY DUCTS 

common. These attacks by no means warrant a diagnosis of suppura- 
tion of the biliary tract, although they are evidences of infection. This 
chronic catarrhal cholangitis may lead to suppurative cholangitis (of 
which it is often only a minor manifestation), acute infectious jaundice, 
acute yellow atrophy of the liver, etc. 

Diagnosis. — In cases of persisting jaundice that begin seemingly as 
acute catarrhal cholangitis, one must attempt to eliminate cholelithiasis 
and malignant disease obstructing the ducts. Often it is quite impos- 
sible to differentiate non-calculous from calculous cholangitis with a 
gallstone in the common duct; attempts to do so are usually only .of 
academic interest. A history of antecedent gallstone colic is suggestive, 
but by no means conclusive. Hypertrophic biliary cirrhosis may be 
eliminated by the absence of marked enlargement of the liver and spleen. 

Prognosis. — The prognosis is dependent upon the associated lesions. 

Treatment. — The treatment is essentially that of acute catarrhal cho- 
langitis. In protracted cases operation should be undertaken with a 
view to drain the biliary ducts; this is the more urgently demanded in 
view of the impossibility often of excluding obstruction due to a gallstone. 



ACUTE CHOLECYSTITIS. 

Etiology. — It is largely artifice that leads to a distinction between 
cholangitis and cholecystitis; the one like the other is an expression of 
infection of the biliary tract. In some cases the infection may remain 
confined to the ducts or the gall-bladder. In other cases, developing in 
the one or the other, the process may extend to that not primarily in- 
volved; and it may persist in the gall-bladder and subside in the ducts, 
or vice versa. 

Acute cholecystitis may result from the microorganisms already men- 
tioned as causative of acute cholangitis. Special importance attaches 
to Bacillus typhosus, Bacillus coli, and the pyococci. These usually 
reach the gall-bladder by way of the portal circulation, less commonly 
by way of the general systemic circulation, and sometimes, perhaps, by 
way of the diverticulum of Vater. Important contributing factors com- 
prise those that reduce the vitality and resisting power of the gall-bladder 
and those that interfere with the free flow of bile. 

Significance attaches to the fact that the gall-bladder once having 
become infected, may harbor the invading bacteria for many years 
(so-called "chronic carriers," especially important in relation to typhoid 
fever); these bacteria being continuously or intermittently discharged 
from the gall-bladder, are often the source of epidemics. 

Pathology. — Various types of acute cholecystitis may be differentiated 
— catarrhal, suppurative, phlegmonous, gangrenous, and membranous. 
Properly interpreted, these are varying manifestations of the one process 
(an infection), which results from variations in the virulence of the in- 
fecting agent, in the local and general resistance, and in the freedom of 



ACUTE CHOLECYSTITIS 727 

the circulation of the bile; they differ in degree rather than in nature, 
and pass sometimes almost imperceptibly the one into the other. In 
the mild cases the gall-bladder is distended and tense; the wall is swollen, 
cedematous, and softened, and the mucosa is, in addition, congested and 
covered with a layer of mucus, perhaps bile-stained; in many cases the 
inflammatory phenomena invade also the peritoneal covering, which then 
is dull, lustreless, or opaque, and covered with a thin layer of fibrin, 
which may serve to unite the gall-bladder to adjacent structures. The 
cystic duct usually is partially obstructed from swelling of the mucosa; 
sometimes it is completely obstructed, but usually only in the event of 
recurrent attacks of inflammation or of cicatrization of ulcerations. The 
contents of the gall-bladder usually consist of turbid bile. Gallstones 
may be encountered, especially in recurrent attacks; but usually not in 
cases of less than four to six months' duration (during most of which time 
the infection may be latent). The adjacent lymph nodes, especially 
those in the portal fissure, are usually enlarged and softened. The more 
severe cases exhibit all gradations to severe suppurative, ulcerative, and 
gangrenous lesions, with more or less suppurative contents (acute and 
chronic empyema of the gall-bladder). 

Symptoms. — Initial nausea and vomiting, fever, pain, and tenderness 
in the region of the gall-bladder, rigidity of the overlying abdominal 
muscles, and an enlarged and tender gall-bladder constitute the impor- 
tant clinical manifestations of acute cholecystitis. These may be of 
sudden or rather insidious onset. The nausea and vomiting are usually 
moderate in grade and soon subside, except in the event of perichole- 
cystic or more general peritonitis and concomitant paresis of the intestine. 
In catarrhal cholecystitis the fever is slight and lasts only a short time; 
in the cases complicating some general infection there may be little if any 
added fever, but if occurring, for instance, during convalescence from 
typhoid fever, the onset of the cholecystitis is often announced by 
fever, which may be high. The pain usually occurs first in the epigas- 
trium, sometimes directly in the midline, and later becomes more localized 
to the right hypochondrium; it varies much in character, and may be 
colicky. Jaundice is not a part of cholecystitis, but it may occur in the 
event of complicating cholecystitis, or obstruction of the common duct. 

The consequences of acute cholecystitis are many: Persistent mild 
infection (chronic bacillus cairiers) with acute exacerbations; gall- 
stones; pericholecystic adhesions; or progression to severe types of the 
affection, with ulceration and perforation (sudden increase of the local 
pain, more or less collapse, increased pulse rate, and increase of the 
local abdominal symptoms — that is, peritonitis). 

Diagnosis. — The diagnosis of acute cholecystitis presents no serious 
difficulties in the great majority of cases; nausea and vomiting, pain and 
tenderness in the region of the gall-bladder, rigidity of the overlying 
abdominal muscles, and an enlarged and tender gall-bladder constitute a 
complex of symptoms that can scarcely be attributed to anything else. 
The phenomena of gallstone colic are properly attributable in most cases 



728 DISEASES OF THE GALL-BLADDER AND BILIARY DUCTS 

to an acute cholecystitis, perhaps acute exacerbation of a chronic chole- 
cystitis. In the severe cases, with well-marked peritonitis of the upper 
abdomen, one must exclude other causes of such peritonitis, especially 
perforated gastric or duodenal ulcer, acute pancreatitis, etc. 

Prognosis. — In the majority of cases the prognosis is good, the 
process tending to subside, under appropriate treatment, within ten days 
or a fortnight. Sequels, especially gallstones and adhesions, however, 
are almost certain to occur, so that the subsequent outlook is not the best; 
in other cases a low-grade infection may persist and the patient become 
a subject of chronic infection and recurring attacks of cholecystitis. In 
the more severe forms, suppurative, phlegmonous, and gangrenous 
cholecystitis, the tendency toward spontaneous cure is slight; in this 
event the prognosis is grave, since not only are the lesions of the gall- 
bladder serious in themselves, but a localized abscess or general peri- 
tonitis may ensue and a fatal issue result, unless recourse is had to 
surgical intervention. 

Treatment. — The treatment is that recommended for gallstone colic 
(page 735), which virtually is an attack of more or less acute cholecystitis. 
In the severe, suppurative, and gangrenous cases, surgical intervention is 
called for. 

CHRONIC CHOLECYSTITIS. 

Chronic cholecystitis may be the residual manifestations of an acute 
cholecystitis, or the process may be chronic from the beginning. The 
etiological factors, therefore, are those of acute cholecystitis, the chron- 
icity of the process being a manifestation of lingering infection, or the 
consequence of a low-grade infection with almost, but not quite, sufficient 
biliary drainage. In the great majority of cases the condition is asso- 
ciated with gallstones the one process sustaining the other; that is, 
most cases are calculous. In a few cases the lesions extend throughout 
the biliary tract; that is, cholangitis and cholecystitis are associated. 
In the absence of gallstones, the lesions may be catarrhal and the gall- 
bladder may be distended. In most long-standing cases the gall- 
bladder becomes reduced in size, thickened, and sclerotic; it may be 
represented by a mass of thickened, contracted connective tissue, perhaps 
enclosing gallstones. Symptomatically, the condition cannot be dis- 
tinguished with certainty from cholelithiasis. 



CHOLELITHIASIS. 

(Gallstones. ) 

Etiology. — Cholelithiasis is an exceedingly common condition, being 
found at the necropsy in from 5 to 10 per cent, of subjects dead from all 
causes. It occurs at all ages, but the incidence increases progressively 
with advancing years; 75 per cent, or more of the cases are found in 



CHOLELITHIASIS 729 

persons over forty years of age, and less than 1 per cent, in those under 
twenty years; but this age incidence does not correctly represent the 
time of the formation of gallstones, since in many cases, having formed, 
they remain latent for years and are found only when the subject dies at a 
more advanced age from the consequences of gallstones or other causes. 
Doubtless, therefore, many, if not most, gallstones are formed in early 
adult life, before the fortieth year, corresponding with the period of 
greatest frequency of typhoid and other infections. They are more 
common in women than in men (the ratio being variously stated as 5 to 
1 (Schroeder), to 4 to 3 (Rolleston). The essential cause is a low-grade 
catarrhal inflammation of the biliary tract, which is usually provoked 
by the typhoid or colon bacilli, or attenuated pyococci; a contributing 
factor is some obstruction to the free flow of bile. This ensues in con- 
ditions of biliary obstruction, and is promoted by a sedentary life, obesity, 
muscular inactivity, lax abdominal muscles (as after pregnancy), hepato- 
ptosis, etc. Whether a third factor, disorders of metabolism (disorders 
dependent upon diet), is active, has not been determined with certainty. 
Pathology. — Gallstones may be found in any part of the biliary tract, 
but they are most common in the gall-bladder. There may be one or 
many stones; they vary much in size — from the smallest particle (biliary 
sand or gravel) to those larger than a normal gall-bladder; and they 
vary in shape. Single stones are usually ovoid, spheroid, or pear-shaped; 
multiple stones are usually cuboidal or polyhedral, and are faceted 
(from mutual compression). Stones within the intrahepatic ducts con- 
form to the ducts in shape, and are ovoid or cylindrical; occasionally 
they are branched, as are the ducts. Although usually smooth, the sur- 
face of gallstones may be rough, irregular, or nodular (mulberry cal- 
culus). In consequence of the bacterial infection of the biliary tract, a 
low-grade catarrhal inflammation is set up; this, on the one hand, leads 
to obstruction of the free flow of bile from swelling of the mucous mem- 
brane, and the products of this inflammation, on the other hand, contain 
the essential constituents of gallstones. In the gall-bladder the catarrhal 
inflammation leads to desquamation of the lining epithelium, an albu- 
minous exudation, and an increased formation of mucus and of choles- 
terin; and in the gall-bladder dynamic factors frequently favor the stag- 
nation of bile. The increased cholesterin is derived not from the bile, 
but from catarrhal disintegration of the mucous cells lining the wall of 
the gall-bladder. Bacmeister and Exner and Heyrovsky, however, have 
shown that bacteria, notably the typhoid and the colon bacillus (but not 
streptococci), may effect directly a decomposition of the bile with the 
precipitation of cholesterin. Exner and Heyrovsky attribute this to 
decomposition of the bile acid salts (the solvent menstruum), in conse- 
quence of which the normal amount of cholesterin can no longer be held 
in solution. The bilirubin calcium is derived from the bile, being pre- 
cipitated by bacterial growth or by the albuminous exudation of the 
inflammatory process. Bilirubin calcium is believed by Naunyn to act 
as a cement substance, binding together the cholesterin, desquamated 



730 DISEASES OF THE GALL-BLADDER AND BILIARY DUCTS 

epithelium, etc., the whole forming the nucleus of the gallstone. Agglu- 
tinated typhoid and other bacteria also may apparently act as the nucleus. 

The following varieties of gallstones are distinguished by Naunyn: (1) 
Pure cholesterin stones, which consist of nearly pure cholesterin, and are 
uncommon. They vary in size from that of a cherry to that of a pigeon's 
egg, are hard, oval, or roughly spherical, seldom faceted, have a smooth 
or nodular surface, and are pure white or yellowish and translucent, or 
rarely brown, greenish, of brownish-black on the surface. On section 
they are white, and crystalline throughout, or show brown deposits be- 
tween the crystals; they are not stratified. (2) Laminated cholesterin 
stones, which consist of about 90 per cent, of cholesterin, together with 
bilirubin calcium, biliverdin calcium, and calcium carbonate. In general 
appearance they resemble the pure cholesterin calculi, but they may be 
brittle and friable, and they are often faceted. On section, they are 
more or less distinctly laminated, layers of almost pure white alternating 
with others that are yellow, brown, green, or red. The centre may be 
crystalline, but the external layers are usually vitreous or earthy. (3) 
The common (or mixed cholesterin) stones, which vary much in size, 
although they seldom equal a large cherry; they may be small and very 
numerous, and are usually faceted. The surface is usually yellow, but 
often brown or white. When fresh, they are often soft and greasy; when 
dried, they undergo shrinkage and become harder. On section, the 
centre is often soft and may contain a cavity. (4) Mixed bilirubin cal- 
cium stones, which may consist roughly of 75 per cent, of bilirubin calcium 
and about 25 per cent, of cholesterin. They are as large as a cherry, or 
larger, and may occur singly or in groups of three or four in the gall- 
bladder or larger ducts. Their shape depends upon their situation; 
when multiple, they may be faceted. They consist of concentric layers 
of reddish-brown or dark brown material, which is seldom quite hard, 
and contracts on drying, often with the formation of fissures or cracks. 
(5) Pure bilirubin calcium stones, which vary in size from that of a grain 
of sand to that of a pea. There are two types: small, solid, brownish- 
black concretions, with rough, irregular surfaces and wax-like consistency, 
and exhibiting a disposition to become welded; and harder, smooth con- 
cretions of a grayish-black metallic lustre and an internal spongy struc- 
ture. (6) Rarer stones, such as amorphous and incompletely crystalline 
cholesterin gravel (resembling pearls); calcareous stones; concretions 
with included bodies and conglomerate stones; and casts of the bile ducts. 

Symptoms. — The characteristic and significant symptoms are: (1) 
Chronic, long-continued, or recurring indigestion, and (2) the phenomena 
designated gallstone colic. The symptoms of chronic long-continued or 
recurring indigestion are of the utmost importance and are commonly 
misinterpreted. This stands in relationship with the facts — that gall- 
stones are present in very many subjects and are commonly believed not 
to cause noteworthy symptoms (in not more than 5 per cent, of the sub- 
jects); that symptoms, having once occurred, are exceedingly likely to 
recur; and that the symptoms are often paroxysmal and very severe. 



CHOLELITHIASIS 731 

Gallstones are sometimes latent, particularly in elderly subjects, in whom 
the original infection has died out, and in whom more or less atrophy, 
especially of the muscular coat of the gall-bladder and biliary ducts, has 
occurred; but there can be no doubt that symptoms commonly denomi- 
nated "stomach trouble," "indigestion," "dyspepsia," etc., are often 
due to gallstones and disease of and about the biliary tract. 

Gallstone colic usually develops suddenly with severe, often agonizing, 
pain in the right hypochondrium or the epigastrium, radiating around 
the chest or to the right scapular region, nausea, vomiting, and prostra- 
tion — weak, rapid pulse, rapid heart action, profuse perspiration, etc. 
Sometimes the attack is preceded by local, less acute pain or discomfort, 
chilliness, fever, etc.; more commonly (60 per cent, or more of the cases) 
chilliness and fever accompany and follow the pain. In some cases 
the severe pain lasts for a few moments only; usually it lasts from 
two to twelve hours; in unusual cases it may last much longer, but in 
these circumstances the phenomena are more correctly interpreted as a 
succession of paroxysms. Often the pain ceases as suddenly as it began, 
but usually following the agonizing pain, more or less dull aching con- 
tinues for a variable period. The colic may recur at varying intervals — 
days, weeks, months, or years; occasionally there is only one attack; 
usually there are many. With succeeding attacks the likelihood of other 
attacks increases. In some cases the pains are not colicky; that is, the 
classical gallstone colic does not occur. The pains, of whatever nature, 
are usually due to an acute cholecystitis, or reactivation of a more or less 
quiescent cholecystitis; but, as pointed out by Riedel, the colicky pains 
may be due to: (1) Adhesions of a gall-bladder no longer containing 
stones; (2) adhesions when large stones are present in the gall-bladder 
and the cystic duct is patent; (3) inflammatory processes in a gall- 
bladder distended by fluid or stones, when the cystic duct is occluded by 
inflammation or by the presence of a stone in the neck of the gall-bladder; 
(4) the transit of a stone through the bile passages; and (5) the inflam- 
mation of a dilated, calculous common duct or its tributaries, without 
impaction of a stone. 

Jaundice may occur, but is entirely absent in at least one-third of the 
cases. It varies much in degree and duration with the local conditions. 
It may be due to: (1) Gallstones in the hepatic or the common bile duct; 
(2) spasm of the musculature or inflammatory swelling of the mucosa of 
the biliary ducts, and (3) compression of the common duct or of the extra- 
hepatic part of the hepatic duct by a large stone in the cystic duct, 
swollen lymph nodes, regional tumors, inflammatory exudations, adhe- 
sions, kinking of the ducts, etc. The gall-bladder may be enlarged and 
palpable in early cases; but in advanced cases, when the gall-bladder has 
become thickened and cicatrized and is manifestly incapable of dis- 
tending, it is usually not palpable. Courvoisier stated that in cases of 
chronic jaundice, contraction of the gall-bladder is suggestive of gall- 
stones, and that dilatation of the gall-bladder is suggestive of biliary 
obstruction, caused by factors other than gallstones; that is, pressure 



732 DISEASES OF THE GALL-BLADDER AND BILIARY DUCTS 

from without (most often enlargement, carcinoma, of the head of the 
pancreas). This, so-called Courvoisier's law, is applicable in perhaps 
two-thirds of the chronic cases. 

Fever is common, and should be correctly interpreted — as a manifes- 
tation of infection, and not as due to reflex causes, etc. In many cases, 
concurrently with the development of the gallstone colic, there is a sud- 
den elevation of the temperature, followed sometimes by an equally 
sudden fall; in other cases, the fever is of longer duration — obviously 
due to acute cholecystitis, or an acute exacerbation of a chronic chole- 
cystitis; in still other cases, especially cases of calculus in the common 
duct, the fever is that known as Charcot's intermittent hepatic (or biliary) 
fever— periodic attacks of chill, fever (103° to 104°R), and sweats, usually 
accompanied by pain in the epigastrium or right hypochondrium, re- 
currence or increase of jaundice, perhaps nausea and vomiting, and 
often leukocytosis. 

Obstruction of the Cystic Duct. — The calculus is usually lodged 
in the beginning of the duct or in the termination of the neck of the gall- 
bladder. The following conditions may ensue: (1) Acute cholecystitis 
(catarrhal, suppurative, phlegmonous, or gangrenous). (2) Chronic 
dilatation of the gall-bladder, a condition that follows complete obstruc- 
tion to the entrance of bile into the gall-bladder, which soon becomes 
distended with mucus, at first bile-stained, but ultimately quite clear 
(so-called hydrops). (3) Chronic fibrous or atrophic cholecystitis — 
the usual sequel of hydrops when the obstruction is not complete and 
the infection dies out. The gall-bladder gradually lessens in size and 
may ultimately be reduced to a mass of fibrous tissue, which usually 
tightly encircles a calculus. 

Obstruction of the Common Bile Duct. — The obstruction may 
be complete or incomplete, and may or may not be associated with 
cholangitis. When the obstruction is complete, a stone is usually 
tightly impacted in the common duct; when the obstruction is incom- 
plete, the stone may be more or less fixed, but permits the flow of bile 
around it, or it may circulate in the common duct and imitate the con- 
ditions in a ball valve. Dilatation of the biliary ducts usually ensues, and 
to the common cholangitis and pericholangitis more or less fibrosis 
of the adjacent liver tissue and atrophy of the liver cells often ensue — a 
condition sometimes spoken of as obstructive biliary cirrhosis In the 
event of complete obstruction without infection, deep and permanent 
jaundice is produced, and is unattended by fever. Incomplete obstruc- 
tion may last for many years without leading to jaundice. Usually, 
however, jaundice is present; it lasts a long time, varies in intensity 
with the degree of obstruction, is subject to more or less fluctuation, 
which is very characteristic; and there is fever, periodic, intermittent, 
or remittent, or more or less continuous (indicative of the usually asso- 
ciated biliary infection). Osier has emphasized the importance of the 
following signs in the diagnosis of a ball-valve calculus in the diverticu- 
lum of Vater (where it occurs most frequently), or in the common bile 



CHOLELITHIASIS 733 

duct: " (a) Ague-like paroxysms of chill, fever, and sweating — the hepatic 
intermittent fever of Charcot; (b) jaundice of varying intensity, which 
persists for months or even years, and deepens after each paroxysm ; and 
(c) at the time of the paroxysm, pain in the region of the liver, with gas- 
tric disturbance. . . . Pain, which is sometimes severe and colicky, 
does not always occur. There may be vomiting and nausea. As a rule, 
there is no progressive deterioration of health. In the intervals between 
the attacks the temperature is normal." 

Complications and Sequels. — Of the many complications and sequels of 
cholelithiasis, some infectious, some purely mechanical, but most of them 
infectious and mechanical, the following are the most important: (1) 
Infectious {Inflammatory) Lesions of the Biliary Tract and Adjacent 
Viscera. These comprise especially varying grades of acute and chronic, 
suppurative and non-suppurative, cholangitis and cholecystitis, pro- 
gressing perhaps to ulceration, gangrene, perforation, etc. The inflam- 
matory phenomena may extend to adjacent structures, and set up local 
peritonitis (with abscess formation) or a more widespread peritonitis, 
pylephlebitis, pancreatitis, etc. (2) Chronic Pericholecystic Adhesions. 
These represent the sequels of postsubacute and chronic, sometimes 
acute, inflammation that has spread to the adjacent peritoneum. Similar 
adhesions may follow disease of the stomach and duodenum; and any 
of these adhesions may be responsible for "stomach ache," "indigestion," 
"biliousness," etc. (3) Biliary Fistulas. Fistulous communications be- 
tween the biliary tracts and adjacent viscera, as well as the exterior of the 
body, frequently result from cholelithiasis and the associated inflam- 
matory and ulcerative processes. Courvoisier in a study of 499 cases, 
found that fistulous communications had been established as follows: 
between different parts of the biliary passages in 8; into the portal vein 
in 5; into the peritoneal cavity in 70; into peritoneal adhesions in 49; 
into the retroperitoneum in 3; with the stomach in 13; with the duo- 
denum in 83; with the jejunum in 1; with the ileum in 1; with the colon 
in 39; with the urinary tract in 7; with the pleura and lung in 24; and 
externally in 196. (4) Intestinal Obstruction. This is a rare event, 
that may follow ulceration of a gallstone from the gall-bladder into the 
duodenum, or, less commonly, the colon. The obstruction occurs most 
commonly in the ileum (near the ileocecal valve), and may be suspected 
in a person in advanced life with a history of past gallstones. 

Diagnosis. — The diagnosis of cholelithiasis comprises the recognition 
of the gallstone colic and of the many and varied associated lesions and 
sequels. Severe pain in the epigastrium or the right hypochondrium, 
radiating around the chest or to the right scapula, accompanied by 
nausea and vomiting and enlargement and tenderness of the gall-bladder 
and followed by jaundice and the detection of a gallstone in the feces, 
are characteristic of the passage of a gallstone; but jaundice is by no 
means always present, and the other symptoms may be provoked by 
cholecystitis in the absence of a gallstone ; indeed, with increasing expe- 
rience, it becomes often more and more difficult to say whether or not 



734 DISEASES OF THE GALL-BLADDER AND BILIARY DUCTS 

gallstones are present in certain individual cases of obvious chronic 
biliary infections. Recourse to the arrays is seldom of much diagnostic 
utility, since the cholesterin stones produce scarcely any shadow, usually 
not more than the adjacent liver; in the rare cases of calcium stones, 
more shadow is cast, but this also is obscured by the shadow of the 
liver. 

The severe pain of gallstone colic may be imitated by renal colic or 
intestinal colic; but in renal colic the pain is usually in the back, loin, 
or groin, and radiates down the ureter to the testicle, which may become 
retracted; strangury or frequent micturition is common; the kidney is 
usually tender (the tenderness being in the loin rather than anteriorly in 
the region of the gall-bladder); and the urine subsequently contains 
blood and a proportionate amount of albumin, perhaps crystals or a 
calculus, and pus and epithelium from the pelvis of the kidney; and it 
does not contain bile. Intestinal colic is usually due to some more or 
less obvious cause; the pain is usually about the umbilicus; it radiates 
in different directions, remits and intermits, and subsides with the 
removal of the exciting cause, often with belching or the discharge of 
feces or gas or mucus by the bowel; and there is no localized tenderness 
in the region of the gall-bladder. In lead colic there is, in addition, the 
history of exposure to the poison, a blue line on the gums, anemia, 
basophilic degeneration of the erythrocytes, and perhaps other present or 
past evidences of the intoxication, such as persistent abdominal discom- 
fort or pain and constipation, wrist-drop, etc. When the symptoms, 
especially the pain, are less acute, and do not merit the designation 
gallstone colic, difficulty may be experienced in differentiating disorders 
of the stomach, especially gastric and duodenal ulcer. The persistence 
of jaundice may suggest malignant disease of the ducts or of the pancreas, 
but in cholelithiasis there is less impairment of the general health; there 
is usually periodic variation in the intensity of the jaundice (of much diag- 
nostic importance); and fever, especially intermittent hepatic fever, is 
likely to be present. 

Prognosis. — The prognosis, as a rule, depends more upon the associated 
conditions than upon the mere presence of the gallstones. The prog- 
nosis in gallstone colic is virtually that of a more or less acute cholecys- 
titis; the outlook as regards permanent health depends upon the chronic 
gall-bladder infection. A first gallstone colic is sometimes the last and 
the infection subsides. Usually, however, there are subsequent attacks, 
if not of severe colic, of more or less disturbance with digestion, and 
general impairment of health due to the toxic absorption, etc.; some 
subjects pass into chronic invalidism from unrecognized chronic biliary 
infections. The occurrence of intermittent hepatic fever, especially of 
severe ague-like paroxysms, renders the prognosis bad, since it shows 
active infection, which, although it may persist for years without sup- 
puration, may nevertheless lead to serious consequences. The prog- 
nosis as to final recovery of health is bad without operative intervention 
in pericholecystic adhesions, fistulse, and intestinal obstructions. 



CHOLELITHIASIS 735 

Treatment. — The fact that gallstones are most common in women, in 
the obese, in those that lead a sedentary life, eat too much, are consti- 
pated, and addicted to alcohol, suggests the correction of certain very 
obvious etiological factors. Women who have been repeatedly preg- 
nant and have lax abdominal walls should wear proper supports. Men 
and women who lead a sedentary life should take properly regulated 
exercise; they should practise deep breathing (to promote the move- 
ments of the diaphragm), bathe frequently, be much in the open air, 
etc. ; that is, they should apply to themselves the general principles of 
hygienic living. Constipation should be overcome, and the diet should 
be such as will be presently pointed out. 

When gallstones have formed, the main indications for treatment may 
be said to be: (1) To cause solution of the stone or stones; (2) to cause 
the discharge of the stone or stones; and (3) to treat the complicating 
infection. 

It is quite impossible to cause solution of gallstones in the gall-bladder, 
olive and other oils, turpentine, ether, etc., being without effect in this 
regard. The many stones said to have been passed by the bowel after 
the administration of olive oil are merely masses of saponified oleic acid, 
resembling gallstones in outward appearance. Olive oil, however, is 
often of service in relieving the commonly attendant hyperchlorhydria. 
To attempt the discharge of gallstones from the gall-bladder, even were 
this possible to effect, is not a worthy object of rational treatment. The 
special function of the physician is to treat the associated biliary infection. 

The fain of gallstone colic is usually so severe as to require the admin- 
istration of morphine, which not only relieves the pain (and mitigates the 
attendant shock), but, by relaxing the spasm of the biliary musculature, 
favors the exit of bile from the tense gall-bladder and the transit of the 
calculus through the ducts (if it be already therein). Usually, \ grain 
(0.015 gram) with -£$ grain (0.0013 gram) of atropine, or yj-g- (0.0006 
gram) grain of nitroglycerin suffices; sometimes after the lapse of fifteen 
to thirty minutes a second smaller dose may seem necessary, but in these 
circumstances a few whiffs of chloroform, or spirit of chloroform or of 
ether (1 dram, 4 c.c), to which tincture of belladonna (5 to 10 minims, 
0.3 to 0.6 c.c), may be added, will usually carry the patient through 
the painful period until the morphine has had time to act; or, and this 
is often attended by excellent results, an additional dose of atropine 
(tot g ram > 0.0006 gram) may be administered hypodermically. Should 
resort be had to chloroform inhalation, one should not induce complete 
anesthesia in the hope of thus relaxing the biliary musculature and freeing 
the calculus; such objects are not thus achieved. In many cases relief 
may also be afforded by hot fomentations over the region of the gall- 
bladder and by lavage of the stomach with water as hot as can well be 
borne. Should the vomiting persist and be manifest especially by inef- 
fectual retching, resort should be had to lavage, if it has not been pre- 
viously used ; sodium bicarbonate may be added to the hot water. The hot 
full bath may also be resorted to at the very beginning of the attack, with 



736 DISEASES OF THE GALL-BLADDER AND BILIARY DUCTS 

hope of excellent result. In other cases the vomiting may be relieved 
by bismuth, carbolic acid, creosote, dilute hydrocyanic acid, cerium 
oxalate, sips of hot water and brandy, champagne, etc. In some cases 
the pain leads to extraordinary depression of the patient, which, if it is 
not relieved by the morphine, should be met with whisky or brandy in 
hot water, or the hypodermic use of camphor. 

Upon the subsidence of the pain, as well as in the absence of a definite 
gallstone colic, the medical treatment of cholelithiasis is that of the 
chronic biliary infection. The diet should be regulated; large amounts 
of an alkaline water should be taken, and the saline cathartics should be 
administered daily./ Salicylic acid seems to augment the flow of bile by 
stimulating its production, and since it also possesses antiseptic properties 
and is excreted with the bile, it exerts a most desirable influence on the 
biliary infection. No preparation is better than chemically pure sali- 
cylic acid; it may be combined with an equal amount of sodium bicar- 
bonate or sodium benzoate; or the salicylates or other preparations of 
salicylic acid may be given, y 

Hexamethylenamin also is excreted in the bile and through the wall 
of the gall-bladder, and serves to disinfect the biliary passages. It 
should be given in generous dose — 40 to 60 grains (2.5 to 4 grams) — 
within twenty-four hours, from time to time; but its general effect should 
be carefully observed. Oxgall also stimulates the secretion and out- 
pouring of bile, and thus favors drainage of the biliary tract; it should 
be administered as salts of the bile acids, such as sodium glycocholate, 
10 to 15 grains (0.6 to 1 gram) daily. Ammonium chloride also is 
sometimes extolled for its effect upon inflamed mucous membranes; by 
promoting the free flow of thin bile it may assist in the much desired 
flushing of the biliary tract. 

Surgical treatment is indicated in all cases in which quiescence or 
latency of the infection cannot be brought about by medicinal measures; 
in the event of recurring attacks of gallstone colic; in the cases that run 
their course under the guise of "indigestion," "biliousness," etc., and in 
which recurrence of attacks is common; in cases of persisting jaundice, 
with or without Charcot's biliary intermittent fever; and in all cases of 
complicating or severe suppurative, ulcerative, or gangrenous chole- 
cystitis. 

CARCINOMA OF THE GALL-BLADDER AND BILIARY DUCTS. 

Carcinoma may develop in any part of the biliary tract, but it is most 
common in the gall-bladder. It is usually associated with gallstones, 
commonly involves the fundus, and may be a fungus-like or an infil- 
trating growth (cylindrical or cuboidal cell). Extension to the liver 
occurs in more than 50 per cent, of the cases. In the biliary ducts 
carcinoma is most common in the common duct, but may occur any- 
where, even in the ampulla of Vater (choledochopancreatic duct); it is 
usually an infiltrating growth. 



HEMORRHAGES INTO THE PANCREAS 737 

Symptoms. — The symptoms of carcinoma of the gall-bladder consist 
usually of antecedent phenomena referable to cholecystitis and chole- 
lithiasis, to which become added a progressive, irregular, and nodular 
enlargement of the gall-bladder (more than one-half of the cases), 
jaundice (three-fourths of the cases), and impairment of the general 
health — emaciation, anemia, and cachexia. Ascites occurs in about 
one-fourth of the cases, being due to portal obstruction or perihepatitis. 
In carcinoma of the extrahepatic biliary ducts, jaundice is usually the 
first noteworthy symptom; it is progressive, soon becomes extreme, and 
is permanent. The stools become acholic. The gall-bladder becomes 
enlarged (smooth, pear-shaped), and metastasis may occur to the liver 
(palpable nodules), to the portal lymph nodes (causing ascites), etc. ; and 
the patient becomes cachectic. 

Prognosis. — Death usually occurs within six months of the onset of 
serious symptoms. 

Treatment. — The treatment is essentially surgical. 



DISEASES OF THE PANCREAS. 

Pathological Physiology. — Some reference has been made in the intro- 
ductory remarks on diseases of the intestine to the pathological physi- 
ology of the pancreatic juice, and, under diabetes, to disturbances in the 
internal secretion of the pancreas. The chief results of disturbances 
(deficiency) of the pancreatic juice consist of imperfect tryptic digestion 
— the occurrence of unchanged muscle fibers in the stools (azotorrhoea), 
especially the non-digestion of the muscle fiber nuclei (Schmidt's test); 
imperfect digestion of carbohydrates, due to lessening or absence of pan- 
creatic amylase; and imperfect fat-splitting, due to lessening or absence 
of steapsin. The stools are voluminous; pale, grayish, slate-colored, or 
clay-colored; pasty, fetid, and acid. The fat content may be as high 
as 80 or 90 per cent, (steatorrhea), instead of the normal 7 to 10 per 
cent. In addition, the urine may contain sugar, rarely a fat-splitting 
ferment (Opie), or it may reveal the so-called Cammidge reaction. 

HEMORRHAGES INTO THE PANCREAS. 

Hemorrhage into the pancreas occurs in a variety of conditions such as 
determine hemorrhage in other organs — infectious diseases, sepsis, hem- 
orrhagic diathesis, purpura, in association with tumors and cysts, and 
following traumas. In addition, however, there is a class of cases in 
which hemorrhage into the pancreas constitutes the only noteworthy 
lesion at necropsy in cases of sudden death occurring in persons pre- 
viously healthy — so-called pancreatic apoplexy. Many of these are 
doubtless cases of hemorrhagic pancreatitis, being reported in the older 
literature, when observations were more or less imperfect and the nature 
47 



738 DISEASES OF THE PANCREAS 

of hemorrhagic pancreatitis ill understood. From these, however, may 
be separated cases occurring in atheroma, and in association with throm- 
bosis and embolism. Symptomatically, however, they cannot be differ- 
entiated from acute or hemorrhagic pancreatitis. 



ACUTE PANCREATITIS. 

Etiology. — Acute pancreatitis is most common in adult males, although 
it occurs in women and has been observed even in infants. Some of the 
patients have given a history of addiction to alcohol ; others have suffered 
from gastro-intestinal derangements, cholelithiasis, or diabetes mellitus. 
In most cases the disease is associated with cholelithiasis and concomitant 
infection of the biliary tract. Usually the gallstone obstructs the com- 
mon bile duct, and thus permits the ready access of the bile to the pan- 
creas. Flexner, Pearce, and others have demonstrated that the injecting 
of bile, artificial gastric juice, and other irritating substances, into the 
pancreatic duct may cause pancreatitis, even in the absence of bacterial 
infection. In some cases ulcerative and suppurative processes of adja- 
cent organs or of remote organs (by metastasis) may set up the pancreatitis. 

Pathology. — Since the time of Fitz's original observations it has been 
customary to distinguish three varieties of acute pancreatitis — hemor- 
rhagic, suppurative, and gangrenous. In many cases, however, it is 
impossible to differentiate between so-called pancreatic hemorrhage, 
hemorrhagic pancreatitis, and gangrenous pancreatitis, and in most 
cases these are but different stages or varying manifestations of the 
one disease. In hemorrhagic pancreatitis the pancreas is enlarged, 
softened, and mottled, dark reddish brown or black in color — the result 
of infiltration of the interstitial tissue with blood. In some cases the 
hemorrhagic infiltration extends also to the neighboring peripancreatic 
tissues, and the mesentery, mesocolon, and omentum. An essential 
feature of the disease is extensive necrosis of all the constituents of the 
gland — the parenchyma, the interstitial tissue, and the bloodvessels, 
with which inflammatory phenomena (polynuclear leukocytic infiltra- 
tion and serofibrinous exudation) are associated. The hemorrhage is 
attributed to necrosis and consequent rupture of the bloodvessels. The 
necrotic foci are sharply demarcated from the surrounding living tissue 
by a narrow zone of reactive inflammation. Opie draws attention to the 
occurrence of hyaline thromboses within the relatively intact tissue 
adjoining the necrotic zones, and he believes that " it is not improbable 
that the ferments of the pancreatic juice, notably trypsin, acting upon 
cells injured by contact with various irritant substances which can 
produce hemorrhagic pancreatitis, have a part in the production of the 
widespread disintegration of the parenchyma which results." 

Gangrenous pancreatitis follows hemorrhagic pancreatitis, and no 
sharp line of demarcation can be drawn between them. The initial 
lesions are similar to those of hemorrhagic pancreatitis — necrosis and 



ACUTE PANCREATITIS 739 

consequent hemorrhage; inflammatory alterations soon develop, and in 
the course of time, concurrent with bacterial invasion, the appearances 
recognized as gangrene result. The pancreas is swollen, soft, friable, and 
mottled grayish-black (slate-colored) or reddish brown or black in 
color. In some cases it consists of a dark, mottled, slate-colored, foul- 
smelling necrotic mass; whereas, in a few cases, late in the course of 
the disease, it may consist of a rather firm and dry mass covered with blood. 
Inflammation of the lesser peritoneal cavity results, and is often followed 
by the development of a large abscess cavity containing dark, grumous, 
malodorous, chocolate-colored, purulent material, and in some cases 
the partly or fully sequestered gangrenous pancreas. Rupture of the 
abscess into the intestine may ensue. 

Suppurative pancreatitis is a secondary condition, and not the cause 
of the gangrene. There may be a single large abscess or many small 
abscesses — the pancreas being correspondingly enlarged and softened. 
The suppuration may extend to the adjacent tissues, or rupture may 
occur into the lesser peritoneal cavity (giving rise to a large abscess 
cavity), or into the stomach or the duodenum; or pylephlebitis and liver 
abscess may result. 

Fat necrosis is a common concomitant of acute hemorrhagic and 
gangrenous pancreatitis, and may be observed also in association with 
chronic suppurative and chronic interstitial pancreatitis. It occurs 
as disseminated or multiple minute foci in or upon the pancreas, and as 
larger foci (2 to 3 mm. in diameter) in the fat of the omentum, and of 
the subperitoneal and retroperitoneal tissues, and sometimes in the peri- 
cardial and subcutaneous fat. Extremely large foci have occasionally 
been observed. The foci are whitish or yellowish and opaque (in marked 
contrast to the translucent yellow of the normal fat), and they are fre- 
quently surrounded by a narrow zone of hemorrhage. They consist of 
lime and certain fatty acids. Flexner has demonstrated the presence 
of the fat-splitting ferment (presumably that of the pancreatic juice) 
in distant necrotic foci (subcutaneous and peritoneal fat), as well as 
in the foci in the immediate vicinity of the pancreas. Fat necrosis 
is believed to result from diffusion of the pancreatic ferment in conse- 
quence of hemorrhagic destruction of the gland or obstruction of the ducts. 

Symptoms. — As a rule, the patient presents a history of long-standing 
gastro-intestinal derangement; sometimes of more or less distinct and 
recurring attacks of colicky pain, nausea, and vomiting, attributable in 
some cases to cholelithiasis, in others, perhaps, to minor attacks of pan- 
creatitis from which the patient has recovered. Acute pancreatitis 
itself is characteristically acute in onset, with sudden, severe, continuous 
pain in the epigastrium, nausea, and vomiting, soon followed by collapse, 
subnormal temperature, rapid pulse, and sometimes death within twenty- 
four to forty-eight hours. The pain, though continuous, is subject to 
paroxysmal exacerbations, and is intensified by motion and vomiting; 
as a rule, it is not very well localized — spreading from the epigastrium 
over the upper part of the abdomen (doubtless due to stretching and 



740 DISEASES OF THE PANCREAS 

tearing of the coeliac plexus). Occasionally the pain is more marked to 
the left of the median line — when the lesions are more marked in the 
tail of the pancreas. The epigastrium is exquisitely tender, especially 
on deep pressure. Should the patient not die, evidences of peritonitis 
of the upper part of the abdomen soon develop. The pain and tender- 
ness continue; rigidity of the abdominal muscles becomes marked; and 
distention, due to paresis of the stomach and intestine, ensues. The bowels 
are markedly constipated (whence the condition may be mistaken for 
intestinal obstruction), the temperature rises and may reach 104° F. 
(though this is unusual), the pulse becomes rapid and thready, hiccough 
and thirst may increase the distress of the patient, the features become 
pinched and pallid, the expression anxious, and some mental wandering 
and delirium may supervene. Physical examination may disclose a 
deep-seated swelling or merely induration — tympanitic on percussion 
because of the overlying stomach and intestine. A chill sometimes occurs 
at the onset, but is more common and is likely to be repeated later, 
and to be associated with sweating and leukocytosis, when suppura- 
tion has supervened. Slight jaundice is observed in some cases, and 
is attributed to obstruction of the common bile duct or this and the 
pancreatic duct by a gallstone in the diverticulum of Vater, by swelling 
of the duodenal mucous membrane, by the enlarged and swollen pancreas, 
or by an abscess which may develop. The urine is lessened in amount, 
and may contain albumin and casts, but rarely sugar. Opie has sug- 
gested that the fat-splitting ferment may be found in the urine in some 
cases and recommends this as a test of possible diagnostic value. An 
abscess may rupture into the intestine, and blood and pus, and even a 
portion of the necrotic pancreas, may appear in the stools. If the disease 
is not fatal within several days, the acute symptoms subside, and rarely 
the patient may eventually recover or the disease may become chronic. 
Usually, however, if not relieved by operation, the patient dies from 
exhaustion and sepsis in the course of several days or weeks. 

Diagnosis. — "Acute pancreatitis is to be suspected when a previously 
healthy person or a sufferer from occasional attacks of indigestion 
is suddenly seized with a violent pain in the epigastrium followed by 
vomiting and collapse, and in the course of twenty-four hours by a 
circumscribed swelling, tympanitic or resistant, with slight elevation of 
temperature. Circumscribed tenderness in the course of the pancreas 
and tender spots throughout the abdomen are valuable diagnostic signs" 
(Fitz). The different forms of acute pancreatitis cannot be differentiated 
the one from the other, though suppuration is suggested by the ordinary 
evidences of sepsis. Other causes of peritonitis in the upper part of the 
abdomen should be taken into consideration, but it is often impossible 
to differentiate before operation, perforation of a gastric or a duodenal 
ulcer, though the history sometimes affords a clue. In cholecystitis the 
pain is less severe, is located over the gall-bladder, and radiates to the 
right and the back; muscular rigidity is less widespread; and tympany, 
if it occurs, is delayed and less marked. A history of previous biliary 



CHRONIC PANCREATITIS 741 

colic and jaundice is inconclusive, since it may be present in pancreatitis 
as well as in cholecystitis. Irritant (and ptomaine) poisoning is suggested 
by the history of the case, analysis of the vomit, generalized abdominal 
pain, and diarrhoea (as contrasted with constipation). 

Treatment — The nature of the disease precludes the possibility of 
medicinal treatment being of much avail. At the onset, attempts should 
be made to relieve the pain by hot fomentations locally and morphine 
hypodermicly, and to counteract the collapse by stimulants and 
external heat. The treatment of the disease itself is essentially surgical — 
exploration and drainage of the lesser peritoneal cavity. In some cases 
this may be undertaken with hope of ultimate success, if the patient 
survives the initial shock. The supervention of suppuration, of course, 
calls for operative intervention. 



CHRONIC PANCREATITIS. 

Etiology. — Chronic interstitial pancreatitis (fibrosis of the pancreas) 
is more common in men than in women, especially between the fortieth 
and the sixtieth year (two-thirds of the cases). Its etiological factors 
are: (1) Bacterial infections, the consequence of ascending infection 
of the ducts from the duodenum, or of infection transported by the 
bloodvessels or the lymphatics, as in syphilis, tuberculosis, etc. (2) 
Intoxications, especially alcohol, probably answerable for the rather 
common association of interstitial lesions in the pancreas and cirrhosis 
of the liver. (3) Mechanical factors. Opie, who has studied the 
subject attentively, states that "the most common cause of chronic 
pancreatitis is obstruction of the duct of Wirsung, due to pancreatic 
calculi, to biliary calculi in the terminal part of the common bile duct, 
or to carcinoma invading the head or body of the gland. Obstruc- 
tion of the duct may be followed by the invasion of bacteria, and 
these take part in the production of the resulting lesion. Ascending 
infection of the unobstructed duct of Wirsung may follow an acute lesion 
of the duodenum or of the bile passages, and may cause chronic inflam- 
mation. In cases which give a history of long-standing vomiting, chronic 
diffuse pancreatitis may be found at necropsy, and is probably the 
result of an ascending infection of the gland. " 

Pathology. — The noteworthy lesion consists of enlargement and 
induration of the head of the pancreas, in some cases of the entire 
organ. Opie distinguishes two varieties of chronic pancreatitis: (1) 
Interlobular pancreatitis, the result of obstruction of the ducts, and 
sometimes of ascending infection, and characterized by proliferation 
of connective tissue between the lobules, only secondary invasion of 
the lobules, and non-implication of the islands of Langerhans, except 
in a very advanced stage of the disease; and (2) interacinar (or intra- 
lobi^ar) pancreatitis, much less common than interlobular pancrea- 
titis, and characterized by proliferation of the interacinar connective 



742 • DISEASES OF THE PANCREAS 

tissue with early invasion and hyaline degeneration of the islands of 
Langerhans. This accompanies atrophic or Laennec's cirrhosis of the 
liver, arteriosclerosis, and hemochromatosis. A congenital syphilitic 
pancreatitis, characterized by diffuse interstitial connective-tissue hyper- 
plasia and atrophy of the parenchyma, but with preservation of the 
islands of Langerhans, is also described. 

Symptomatology. — The symptoms of chronic pancreatitis are quite 
obscure, and in many cases the condition is merely an interesting 
finding at the necropsy. Occasionally, however, local symptoms 
due to the situation of the organ, evidences of interference with the 
motility of the stomach and duodenum, and disturbances with the func- 
tions (the internal and the external secretions) of the gland, permit an 
inference as to the presence of chronic inflammatory alterations. The 
symptoms develop insidiously, rarely following an acute attack, and 
consist of gradually increasing dyspepsia, loss of appetite, nausea, 
flatulence, and epigastric distention. Deep-seated pain, tending to 
radiate to the left and the back, is occasionally complained of, and on 
palpation, deep-seated tenderness and sometimes a sensation of increased 
resistance, corresponding to the pancreas, may be elicited. Vomiting 
sometimes results from motor insufficiency and dilatation of the stomach, 
induced by enlargement and induration of the head of the pancreas ; occa- 
sionally it is frequent and persistent. Jaundice, which may be slight or 
marked and prolonged, is common also in conditions of enlargement and 
induration of the head of the pancreas (as well as in tumor formations), 
and results from obstruction of the common bile duct. Some cases of 
so-called catarrhal jaundice have been attributed by Mayo Robson to 
enlargement of the head of the pancreas. Obstruction of the portal 
vein may lead to the development of ascites. Glycosuria and other 
evidences of diabetes mellitus occur in a few cases — especially when 
the islands of Langerhans are destroyed; and since this may happen 
without much involvement of the glandular structure of the organ, 
disturbances of pancreatic digestion in the intestine may be absent in the 
presence of glycosuria. Alimentary glycosuria has been observed in many 
cases. The stools are voluminous and contain undigested muscle fibers 
(azotorrhcea) and visible fat (steatorrhcea), but azotorrhoea is found also 
in conditions, such as obstruction of the ducts, from a tumor, a cyst, or a 
calculus, interfering with the flow of the pancreatic juice into the intestine; 
and steatorrhcea occurs in obstruction of the bile duct as well as the pan- 
creatic duct, and after the ingestion of large quantities of fat. The chemical 
constitution of the fat, however, may be of some diagnostic value, since the 
investigations of Mliller seem to show that normally (as well as in conditions 
causing deficiency or absence of bile from the intestine) 75 per cent, of 
the fat in the feces is split up into fatty acids and soaps, whereas in dis- 
ease of the pancreas (causing deficiency or absence of the pancreatic 
juice in the intestine) the fat is present largely as free neutral fat. It 
has been suggested that in such cases a useful test of the presence 
or absence of the pancreatic juice might result from the giving of pan- 



CYSTS OF THE PANCREAS 743 

creatic preparations with the subsequent disappearance from the stools 
of unchanged muscle fibers and fat. However, a marked difficulty in 
the diagnosis of pancreatic disorders consists in the fact that the functions 
of the pancreas are shared by other organs. Diarrhoea is rather common; 
secondary anemia and emaciation are features of some cases; the skin 
may become pigmented; and profuse salivation (pancreatic sialorrhcea) 
occasionally occurs and may become distressing. 

Diagnosis. — The diagnosis is always difficult, and frequently is scarcely 
more than a surmise. The most trustworthy symptoms consist of 
chronic indigestion, more or less jaundice, a disposition to diarrhoea 
and large stools, and emaciation. Carcinoma of the pancreas, carcinoma 
of the bile ducts, a calculus in the common bile duct, and perigastric 
adhesions (following gastric ulcer or carcinoma), must be considered in 
the differential diagnosis. 

Prognosis. — The outlook is good in the event of surgical intervention. 

Treatment. — The treatment, aside from operative intervention, is 
largely hygienic and dietetic. Diastatic ferments, or pancreatic prepara- 
tions, are sometimes of service in aiding digestion. The causative factors 
should receive attention in all cases. Of these, gallstones are of prime 
importance — whence the good effects of operative intervention (drainage 
of the biliary ducts as a preventive, as well as a curative measure). 



CYSTS OF THE PANCREAS. 

Cysts of the pancreas are about equally common in the two sexes — of 
121 of the 134 cases collected by Oser, 60 were in men, and 61 in women. 
Sixty-two of the cases (51 per cent.) occurred between the ages of twenty 
and forty years, but the greatest number (21 cases) occurred in men during 
the fourth decade, and the greatest number in women (21 cases) during 
the third decade. The condition, however, has been observed in infancy. 
Korte distinguishes three varieties : (1) Traumatic cysts, following blows 
and oft-repeated pressure on the abdomen; (2) postinflammatory 
cysts; and (3) cysts of unknown origin. Mayo Robson distinguishes 
anatomically: (1) Retention cysts; (2) proliferation cysts — cystic ade- 
noma and epithelioma; (3) hydatid cysts; (4) congenital cysts; (5) 
hemorrhagic cysts; and (6) pseudocysts. The cyst may develop from any 
part of the pancreas, though probably most frequently from the tail, 
and it varies much in size and in situation in different cases. It may be 
single or multiple, and microscopic in size or so large as to accommodate 
many liters of fluid (a cyst containing 14 liters has been reported). The 
fluid contents is usually slightly opaque and straw-colored, though in 
traumatic cases it may be hemorrhagic. Its reaction is alkaline; its 
specific gravity varies between 1007 and 1028 (Oser); and microscopicly 
it contains fat granules, cell detritus, blood-coloring matter, and 
sometimes cholesterin. Occasionally, but often not in the older cases, 
the fluid digests albumin and fibrin (important), and emulsifies fat and 



744 DISEASES OF THE PANCREAS 

converts starch into glucose (of relatively little importance, since other 
fluids of the body sometimes possess the same qualities). Most cysts 
develop in the lesser peritoneal cavity, displace the stomach upward and 
to the right, and present between the stomach and the transverse colon; 
in some cases the cyst presents above the stomach, which it displaces 
downward; occasionally it develops in the transverse mesocolon and 
presents below the colon; and in still rarer cases it presents toward the 
splenic or the nephritic region. 

Symptoms. — The early symptoms vary, depending on the etiology. In 
traumatic cases, initial pain, tenderness, and vomiting, as well as other 
evidences of local inflammation may be present. In other cases the 
early symptoms are more mild and not to be differentiated from the 
symptoms of chronic pancreatitis. In most cases the presence of a cyst 
is not suspected until it begins to cause enlargement of the abdomen. 
Clinically the cyst appears as a spheroidal, smooth, rather resistant, 
usually immobile mass, presenting in the hypochondriac region between 
the stomach and the colon, though, as already mentioned, it may present 
below the colon — hence below the umbilicus. Other symptoms result 
from the absence of the pancreatic juice from the intestine (azotorrhcea, 
steatorrhea), as well as glycosuria. Certain symptoms result from press- 
ure of the cyst or adhesions, such as neuralgic pains from pressure on the 
regional nerves, jaundice from obstruction of the common bile duct, diffi- 
culty in emptying the stomach and consequent dilatation of the stomach 
from obstruction of the pylorus or the duodenum, ascites and intes- 
tinal hemorrhage from pressure on the portal or the mesenteric vein, 
oedema of the lower extremities from obstruction of the vena cava, 
hydronephrosis from obstruction of the ureter, etc. Rupture of the cyst 
into the peritoneal cavity, the stomach, or the intestine may result in 
(sometimes) sudden decrease in the size of the abdomen, and watery 
discharges from the bowel. 

Treatment. — The treatment consists of operation — drainage or extir- 
pation of the cyst. 



TUMORS OF THE PANCREAS. 

Of the tumors of the pancreas, in themselves comparatively rare, 
carcinoma is the most frequent, though sarcoma and adenoma have 
been observed. Carcinoma of the pancreas is more common in men 
than in women, and occurs most frequently from the fortieth to the 
sixtieth year, but it has been observed in infancy and in advanced life. 
It is most common in the head of the pancreas, but it may be wide- 
spread or limited to the body or the tail. It may be small or very large, 
and frequently extends to adjacent structures by contiguity of structure, 
and gives metastasis to the regional lymph nodes and the liver. The 
growth is commonly an adenocarcinoma, usually of the so-called scirrhus 
variety. 



PANCREATIC CALCULI 745 

Symptoms. — The early symptoms do not differ essentially from 
those of chronic pancreatitis. Epigastric pain is present in most 
cases, and is often paroxysmal. Jaundice, due to obstruction of the 
diverticulum of Vater or of the common bile duct, is a conspicuous symp- 
tom; it may develop gradually or suddenly, is intense and persistent, 
and is usually associated with enlargement of the gall-bladder (in con- 
trast with an impacted calculus in the common bile duct, in which, in 
consequence of infection and consequent atrophy, the gall-bladder is 
usually small : Courvoisier's law). Other symptoms due to pressure on or 
adhesions to regional structures occur, but these are not different from 
those mentioned in connection with pancreatic cyst, although duodenal 
stenosis and consequent gastric dilatation (with nausea and vomiting) 
is probably the most common. Symptoms due to absence of the pan- 
creatic juice are similar to those mentioned under chronic pancreatitis. 
In a small proportion of cases a tumor is palpable, and sooner or later 
the well-known anemia, emaciation, and cachexia of carcinoma intervene. 

Diagnosis. — In the early stages, and, indeed, in the late stages in many 
cases, the disease is not susceptible of diagnosis. The most suggestive 
symptoms are pain, a palpable tumor, jaundice (with enlarged gall- 
bladder), anemia, emaciation, and cachexia. Carcinoma of adjacent 
viscera (pylorus, liver, colon, etc.) must be considered in the differential 
diagnosis. 

Treatment. — The treatment is purely symptomatic. Cholecystenter- 
ostomy and even removal of the carcinoma have been practised in a few 
cases with good temporary results. 

PANCREATIC CALCULI. 

Etiology. — Pancreatic calculi are rare, scarcely more than one hun- 
dred cases having been reported. It occurs especially between the 
ages of thirty-five and forty-five years, and is apparently much more 
common in men than in women (26 cases in men, and 6 cases in 
women, in Oser's collection). As a rule, the calculi are small, often 
so small as scarcely to be discernible, but very large calculi (up to 2 to 
4 cm. in diameter) have been observed. Usually there is more than 
one calculus, sometimes very many (upward of a hundred or more). 
They may be round, oblong, or irregular in shape, and smooth or rough. 
Usually they are composed of calcium carbonate, either alone or in com- 
bination with calcium phosphate. They are sometimes found in the 
pancreatic ducts at necropsy (a personal observation of my own); 
sometimes they become impacted in the duct of Wirsung, or in the com- 
mon bile duct, or in the diverticulum of Vater. Thus they cause: (1) 
Chronic interstitial pancreatitis with marked overgrowth of the fibroid 
connective tissue and atrophy of the glandular tissue, and sometimes lead 
to dilatation of the ducts and large cyst-like formations, which rarely 
establish fistulous communications with adjacent organs, such as 
the stomach, the intestine, etc. (2) In consequence of secondary infec- 



746 DISEASES OF THE PERITONEUM 

tion, they sometimes lead to abscess of the pancreas. (3) Sometimes, 
analogous to a similar process in the gall-bladder, they are said to result 
in carcinoma of the pancreas. The exact cause of the calculus formation 
is not known, although there is some evidence that bacterial infection 
of the mucous membrane results in their formation — analogous to the 
process in the gall-bladder. Indeed, calculi in the biliary passages and 
in the pancreas are sometimes associated. 

Symptoms. — Pancreatic calculi often occasion few, if any, symptoms, 
especially when they lie dormant. Like gallstones, they produce symp- 
toms when they move on from their place of birth (pancreatic colic), and 
when they produce secondary results in and about the pancreas. 

Pancreatic colic is characterized by sudden severe pain in the epi- 
gastrium, radiating to the left mammary region, the left margin of the 
ribs, and the left shoulder, vomiting, and sometimes collapse. In some 
cases the pain is more diffuse, radiates to both sides, and is not to be 
differentiated from some attacks of gallstone colic. Following the 
attack, pancreatic calculi have occasionally been found in the stools. 
Confirmatory symptoms consist of salivation, hunger and thirst (said to 
come on after the colic), fatty diarrhoea, glycosuria, and other evidences 
of interference with the functional activity of the pancreatic juice. As a 
matter of fact, aside from pancreatic colic, the presence of pancreatic 
calculi is altogether insusceptible of diagnosis, the symptoms being those 
of its results — chronic pancreatitis, pancreatic abscess, etc. In the event 
of marked dilatation of the ducts a tumor may be palpable. 

Diagnosis. — The diagnosis is suggested by epigastric pain (colic) often 
recurring and of obscure causation, and associated with glycosuria, 
and many muscle fibers and marked increase of neutral fat in the stools, 
and the absence of evidence of a newgrowth. The calculi are sometimes 
susceptible of recognition by the arrays. 

Treatment. — The treatment of the colic does not differ from that of 
gallstone colic — hot application to the abdomen, morphine and atropine 
hypodermicly, and partial or complete anesthesia (ether or chloroform) if 
necessary. Impaction of the stone with dilatation of the ducts or abscess 
formation calls for surgical intervention. Otherwise, the treatment 
is that of chronic pancreatitis, which also is largely operative. 



DISEASES OF THE PEEITONEUM. 

ASCITES. 

(Hydroperitoneum.) 

Etiology. — Ascites, the accumulation of serous fluid in the peritoneum, 
may be due to general or local causes. The general causes comprise: 
(1) Those that determine dropsy in other parts of the body, such as 
chronic cardiac disease, sometimes antedated by chronic pulmonary 



ASCITES 747 

disease (such as emphysema), or pleural or mediastinal lesions; and 
(2) anemic and cachectic states, such as high-grade anemia, leukemia, 
chronic nephritis, amyloidosis, etc. The local causes comprise: (1) 
Portal obstruction, such as may occur in cirrhosis of the liver, advanced 
passive congestion of the liver, pylethrombosis, or compression or kinking 
of the portal vein; (2) chronic inflammation of the portal vein, tuber- 
culosis or so-called simple; (3) abdominal tumors, such as carcinoma 
of the peritoneum, ovarian tumors, the enlarged spleen of leukemia, etc. 

Symptoms. — The chief manifestation consists of a uniform or sym- 
metrical enlargement of the abdomen. Secondary symptoms, due largely 
to embarrassed cardiac and pulmonary action from compression, are 
usually also present. 

Examination reveals the abdomen to be more or less enlarged. In the 
recumbent posture, there is bulging of the flanks; the umbilicus may 
protrude; the superficial veins are often dilated and tortuous; the anas- 
tomosis between the epigastric and the mammary veins may carry the 
blood upward; in cirrhosis, a plexus of veins may centre in the umbilicus 
(caput medusae). Percussion reveals dulness in both flanks and low 
down in the hypogastric and the inguinal regions, and tympany above 
— around the umbilicus; both the dulness and the tympany shift with 
change in the posture of the patient. Palpation reveals a distinct sense 
of fluctuation (which must not be confounded with a somewhat similar 
sensation transmitted by a fat and relaxed abdomen). 

Diagnosis. — The diagnosis, as a rule, is readily made. One must ex- 
clude ovarian cyst, pancreatic cyst, a distended urinary bladder, and fluid 
feces in a dilated colon. 

The fluid is usually pale amber in color, clear, somewhat opalescent, and 
alkaline. That which occurs in anemic and cachectic states has a spe- 
cific gravity of 1010 or less, and contains less than 1 per cent, of albumin; 
that of obstruction (liver cirrhosis, etc.) has a specific gravity of 1010 to 
1015, and contains from 1 to 3 per cent, of albumin; and that of inflam- 
matory processes (exudates) has a specific gravity of 1015 to 1020 or 
more, and contains from 3 to 5 per cent, or more of albumin. Occa- 
sionally the fluid contains traces of urea, urobilin, purin bodies, sugar, etc. 
Inflammatory fluid is likely also to be turbid. Bacteriological studies show 
the fluid to be sterile, in the absence of infectious processes. Cytological 
studies reveal the cellular constituents of ordinary ascites (transudates) 
to be few and to consist of lymphocytes and endothelial cells, with a few 
erythrocytes and leukocytes; inflammatory fluids may reveal more poly- 
nuclear neutrophilic leukocytes. Cryoscopy reveals the freezing point 
to vary with the amount of albumin. 

Occasionally the fluid is chylous, in consequence of obstruction and 
rupture of the lymphatics (it contains considerable albumin, less than 
0.9 per cent, of fat, and perhaps some sugar); or it may be chyliform 
(no sugar, but considerable fat — 5 per cent, or more); or it may be hemor- 
rhagic (traumatism, rupture of minute vessels, petechial hemorrhages in 
the serous membrane, some forms of tuberculosis, carcinoma, etc.). 



748 DISEASES OF THE PERITONEUM 

The percentage of albumin may be calculated by Reuss' formula — 
the percentage of albumin equals three-eighths of the last two figures of 
the specific gravity, minus 2.8. Rivalta's reaction may also be resorted to 
to differentiate transudates from exudates : to 50 c.c. of distilled water one 
drop of 50 per cent, acetic acid is added, and then one drop of the ascitic 
fluid; in the event of the fluid being inflammatory, on coming in contact 
with the acidulated water, it assumes the form of a bluish- white opalescent 
ring, which, as it broadens out, may become striated by many bluish- white 
lines. 

ACUTE PERITONITIS. 

Etiology. — Acute peritonitis may perhaps occur as a primary disorder, 
but it is very rare. Usually the condition is secondary — to disease of any 
of the abdominal organs; less commonly to diseases of more distant 
organs (by metastasis). The most important antecedent conditions are 
appendicitis, salpingitis, gastric and duodenal ulcer, cholecystitis, and 
pancreatitis; but any inflammatory, suppurative, or ulcerative lesion of 
the gastro-intestinal tract, the female genitalia, the liver, spleen, urinary 
organs, etc., may be followed by peritonitis. The important micro- 
organismal causes are: Bacillus coli, streptococci, staphylococci, Ba- 
cillus pyocyaneus, Diplococcus pneumoniae, Bacillus proteus, Micro- 
coccus gonorrhoea, Bacillus typhosus, etc. ; mixed infections are common. 

Pathology. — The lesions may be circumscribed or diffuse; and fibri- 
nous, serofibrinous, purulent, or hemorrhagic in character; rarely also 
putrid; or there may be only a small amount of thin, serous fluid; or the 
peritoneum may be only opaque and lustreless, no exudate having 
formed. The lesions may extend to the peritoneum from continuity of 
tissue, or from perforation into the peritoneum of a hollow viscus or 
abscess of a solid organ. Special interest attaches to localized peri-appen- 
dicular peritonitis, to pelvic peritonitis (the consequence of antecedent 
infection of the uterus or Fallopian tubes), to peritonitis about the 
pylorus, duodenum, and gall-bladder, and to subphrenic peritonitis. 
From these local lesions the peritonitis may become diffuse; but it may 
become diffuse also with such antecedent localizations as, for instance, 
after perforation in typhoid fever. 

Symptoms. — In the localized forms of peritonitis the symptoms are 
largely those of the antecedent disorder, many of the manifestations of 
which are due to the associated peritonitis. The most important com- 
prise abdominal pain, tenderness, and rigidity of the overlying muscles. 
Nausea, vomiting, and constipation are often present; and there is more 
or less fever, a rapid pulse (sometimes the hard, wiry pulse of the older 
writers), and leukocytosis; and a mass may be palpable. In the per- 
forative cases sudden severe abdominal pain and collapse are usually 
observed. In the diffuse cases the pain and tenderness become more 
widespread, the abdomen distended and tympanitic, and free fluid may 
be more or less readily detected (physical signs of ascites). The pulse 



CHRONIC PERITONITIS 749 

becomes very rapid and weak, and the fever moderate or high (rarely 
only slight fever); nausea and vomiting may persist, and constipation is 
usually obstinate. The face becomes pinched, the eyes sunken, and 
the expression anxious (Hippocratic facies); the skin takes on a pallid, 
cyanotic hue, and may be bathed in continuous or frequently repeated 
sweats; the patient usually becomes delirious, and soon dies. 

Diagnosis. — The diagnosis is usually quite apparent from the afore- 
mentioned symptoms. Special attention should be directed to ascer- 
taining the antecedent condition answerable for the peritonitis. In addi- 
tion to these disorders, in some cases it may be necessary, for a time at 
least, to consider the different types of colic (intestinal, renal, and gall- 
stone), intestinal obstruction, ruptured tubal pregnancy, embolism or 
thrombosis of the superior mesenteric artery, etc. Subphrenic abscess 
usually follows gastric (or duodenal) ulcer or carcinoma, or other suppu- 
rative or ulcerative lesions of the intestine; it is characterized by a collec- 
tion of pus, or of pus and gas (subphrenic pyopneumothorax) between 
the liver and the diaphragm; and it is suggested by severe pain, nausea, 
vomiting, embarrassed respiration, chills, fever, sweats, and leukocytosis, 
and the physical signs of fluid or of fluid and air above the liver. 

Prognosis. — In diffuse peritonitis death usually ensues within forty- 
eight hours. In the circumscribed cases the outlook varies with the 
extent and severity of the lesions and the treatment adopted. 

Treatment. — The treatment, although modified somewhat by the ante- 
cedent disorder, is virtually that described for appendicitis. In the 
majority of cases the treatment is essentially and solely surgical. 

CHRONIC PERITONITIS. 

Etiology. — Chronic peritonitis is perhaps rarely a primary process, in 
which event it is usually set up by the tubercle bacillus. Commonly the 
condition is secondary to disease of any of the abdominal viscera, or it 
may be part of a multiple serositis. 

Pathology. — Like acute peritonitis, the lesions may be circumscribed 
or diffuse. The circumscribed lesions often represent the residue of 
postacute localized peritonitis, and consist of more or less thick or thin 
fibrous adhesions or bands. These are especially common about the 
appendix, the female genitalia, the gall-bladder, pylorus, and duodenum, 
the liver, and the spleen; occasionally they involve the intestine, the 
mesentery, etc. They bind the organs involved to adjacent organs or 
tissues, and more or less seriously interfere with their functional activity. 
The diffuse lesions may consist of: (a) Widespread thickening and adhe- 
sions, which, uniting the intestines to the abdominal parietes and viscera, 
may lead to complete obliteration of the peritoneum (obliterative or 
deforming peritonitis), (b) Serous effusion, which may be slight, 
moderate, or great in amount, and is likely to be tuberculous in nature 
(p. 103). (c) Hemorrhagic effusion, which is most common in tuber- 
culosis or carcinoma of the peritoneum. 



750 DISEASES OF THE PERITONEUM 

Symptoms. — The circumscribed adhesions are responsible for much 
of the so-called chronic ' 'indigestion, " especially the adhesions about the 
appendix, the gall-bladder, the pylorus, and the duodenum. Pain may 
be dull and more or less persistent, or colicky. Eventually more or 
less general impairment of health and invalidism may ensue. A coil 
of intestine may become caught beneath a fibrous band and intestinal 
obstruction and strangulation ensue. 

The diffuse cases with much fluid exudation are characterized by the 
physical signs of ascites; and, since most of the cases are tuberculous, 
there is usually also some fever, local pain and tenderness, and perhaps 
also muscular rigidity, emaciation, etc. A tuberculous focus elsewhere 
in the body may be detectable. Chronic obliterative or deforming peri- 
tonitis is suggested by palpable tumor-like masses and sacculated fluid, 
but it is rarely recognized during life. 

Diagnosis. — The "dyspeptic" cases should be recognized by bearing in 
mind their etiological factors and associated conditions. Ascites and 
fever are significant of the more diffuse lesions (usually tuberculous). 

Prognosis. — Some of the ascitic cases in young subjects tend to undergo 
spontaneous recovery, but in general the outlook in all cases is not 
reassuring. 

Treatment. — The treatment of the tuberculous cases is. mentioned on 
page 105; otherwise the treatment is surgical. 



MULTIPLE SEROSITIS. 

(Multiple Progressive Hyaloserositis, Nicholls; Polyorrhomenitis; Polyserositis; Indu- 
rative Mediastinopericarditis; Chronic Hyperplastic, Hyaline, or Deforming 
Peritonitis; Zuckergussleber; Zuckergussmilz; Zuckergussherz; Zucker- 
gusslunge; Pericardiac Pseudocirrhosis of the Liver, Peck.) 

Etiology. — The cause of multiple serositis is not well understood. Cer- 
tain of the infective diseases, such as typhoid fever, pertussis, malaria, 
syphilis, and rheumatism, are set down as etiological factors in a number 
of the reported cases. In some cases the lesions are of an extremely 
obscure and unknown etiology, whereas in other cases the provoking 
agent is certainly the tubercle bacillus; other cases occur during the 
course of chronic nephritis. 

Pathology. — Anatomically the distinguishing feature of these cases is 
a chronic fibrous (usually hyperplastic) inflammation of the several 
serous membranes of the body — a multiple serositis. In some cases the 
inflammation may remain localized to one or two serous membranes, 
but there is a marked tendency for all the serous membranes to become 
involved. The several serous membranes may become involved equally 
or unequally; usually the lesions are most marked in the pericardium 
and on both sides of the diaphragm. In some cases extensive calcifica- 
tion of the pericardium occurs. In cases in which there is but partial 
obliteration of the pleural or the pericardial sacs there is usually also 



MULTIPLE SEROSITIS 751 

some fluid present. In many cases, however, not only is the pericardium 
thickened and obliterated, but it has also formed adhesions with the chest 
wall and the structures of the mediastinum, one or both pleurae are thick- 
ened and obliterated, and the peritoneum is more or less thickened and 
adherent and contains a large quantity of fluid. In many cases the liver 
is adherent not only to the under surface of the diaphragm, but also to 
the stomach, the colon, the omentum, the anterior abdominal wall, etc. 
The lesions involve also the spleen, especially in those cases in which 
there are extensive adhesions in the left pleura. A distinguishing feature 
of the lesions is the development of thick, fibrous, almost cartilaginous, 
masses of connective tissue, that encase, compress, and often distort the 
organs, and give rise to an appearance suggesting confectioner's icing — 
whence the designation "iced liver," or sugar-iced liver (Zuckerguss- 
leber), etc. In many cases of primary pericarditis the liver is enlarged, 
smooth, and has sharp edges; later, with the development of the peri- 
hepatitis, the liver lessens in size, its surface becomes somewhat irregular, 
its edges rounded, and sometimes the entire organ becomes much dis- 
torted; still later, or in some cases earlier, the appearances characterized 
as nutmeg, with or without atrophic alterations, may supervene. Al- 
though some slight connective-tissue proliferation and some extension of 
newly formed connective tissue from the thickened capsule sometimes 
occur, the common absence of marked connective-tissue proliferation 
in the liver is noteworthy. In some cases the lesions of cirrhosis are 
encountered. 

Symptoms. — Although the disease is characterized by slow, insidious, 
and intermittent course, the perihepatitis and the peritonitis dominate the 
clinical picture of the well-developed disease. Aside from this, that is, 
aside from the ascites, the clinical picture varies, depending upon the 
point of origin of the disease. In some cases the disease is ushered in 
with acute pericarditis, pleuritis (which may necessitate repeated tap- 
pings), or perihepatitis (circumscribed peritonitis), which subsides and 
leaves the patient apparently well for a number of years. Usually, how- 
ever, the lesions of the pericardium and of the pleurae are latent, and the 
first sensible evidence of the disease is ascites. In some cases of primary 
pericarditis slight and transient oedema of the legs may be present 
early, but this is not observed in many cases, inasmuch as the pericar- 
ditis is usually latent. When oedema does occur early, it usually soon 
subsides and does not recur until the ascites has been present for a long- 
time, or until shortly before death; except shortly before death, it is in- 
conspicuous when contrasted with the excessive ascites. Associated 
with early oedema, slight swelling of the spleen and disturbance of the 
gastro-intestinal tract may develop, but these usually subside with the 
ascites, and the disease, as a rule, is characterized by the entire absence 
of such symptoms until shortly before death. The ascites is characterized 
by the fact that it is excessive, that it necessitates repeated tappings, 
that it recurs rapidly after tapping, and that it may remain stationary 
(not necessitating tapping) for many years. After repeated tappings it 



752 DISEASES OF THE PERITONEUM 

may be impossible to draw off much fluid again on account of the devel- 
opment of many adhesions. 

In a few cases lesions of the peritoneum appear to be entirely absent, 
whereas, in other cases they are so slight as to appear inadequate to 
cause the ascites. These may be likened to similar cases of valvular 
disease of the heart, in which disproportionate ascites is the striking 
clinical feature, and in which the ascites is doubtless due directly to the 
congestion of the liver and its consequences, as maintained by Pick. In 
some cases both factors — the congestion of the liver and the peritonitis 
— are operative. In those in which the congestion is the major factor 
we should expect more or less swelling of the spleen and disturbances of 
the gastro-intestinal tract; in those in which the serositis is the major 
factor, we should expect an absence of such symptoms. Some distinction 
— anatomically, at least — may be drawn between cases in which the 
lesions are confined to the peritoneum and cases in which the lesions are 
more widespread. The cases in which the pericardium is unaffected 
reveal no congestive alterations in the liver; clinically, however, the two 
classes of cases are very much alike, and the " Zuckergussleber" may 
occur in both. 

Diagnosis. — Recurring ascites in a person in otherwise good health, 
together with the disposition and ability to be up and about between tap- 
pings, should suggest the diagnosis. Of especial diagnostic significance 
are : a history of a previous attack of pericarditis, pleuritis, or perihepa- 
titis; the early occurrence and subsequent disappearance of oedema of the 
legs; marked ascites with little or no oedema of the legs; an enlarged liver 
early (this may not occur), and a small and distorted but otherwise 
smooth liver late in the course of the disease; the absence or very late 
occurrence of marked enlargement of the spleen; a tendency to the re- 
peated occurrence of attacks of pain, tenderness, rigidity, and possibly 
palpable and audible friction in the right hypochondriac region — attribu- 
table to attacks of perihepatitis; and the rapid recurrence of ascites 
after tapping. One should determine whether the lesions are confined 
to the region about the liver or are more widespread, involving the peri- 
cardium and the pleura. In these cases one must endeavor to dissociate 
the symptoms due to the serositis from those due to failure of the circu- 
lation induced by the pericardial part of the serositis and its consequences. 
In most of these cases prime importance attaches to the recognition of 
an adherent pericardium (page 485). 

From cirrhosis of the liver the condition may be distinguished by the 
signs of adherent pericardium; the absence of the etiological factors of 
cirrhosis of the liver; the slow, insidious, protracted, and intermittent 
course; the long periods during which the ascites may remain stationary 
and the patient in good condition; the entire absence or transient presence 
of slight jaundice; the absence, in most cases, of portal congestion and 
gastro-intestinal disturbances; in some cases, the association of an en- 
larged, smooth, and firm liver, with marked ascites; and the fact that in 
many cases the patient survives a large number of tappings. 



MULTIPLE SEROSITIS 753 

Prognosis. — The prognosis as to eventual recovery is bad, but the 
patient may live for many years. 

Treatment. — The treatment is almost wholly symptomatic. Diuretics 
may effect the discharge of the too abundant fluid or a similar object may 
be achieved by free catharsis. Potassium iodide and mercury may be 
tried when there is a trustworthy history of syphilis, as well as in doubtful 
cases, since they hold out some hope of benefit. Tapping must be 
performed when necessary; usually it has to be done frequently, although 
occasionally the fluid remains at a standstill for long periods of time. 



48 



SECTION IX. 
DISEASES OF THE UEINARY SYSTEM. 



Pathological Physiology. — The kidneys, together with the intestines, 
lungs, liver, and perhaps the skin, are charged with the function of 
excretion; that is, of removing from the body waste products of no 
further use in the economy. Perhaps the kidneys produce also a secre- 
tion, that is, a substance of service in the processes of metabolism; but 
this has not yet been definitely determined. The substances excreted 
by the healthy kidneys are especially the waste products of nitrogenous 
metabolism, certain mineral salts, pigments, and water. All of these 
are normally present in the blood, from which they are removed by the 
healthy kidney — the water and the mineral salts probably by the glomer- 
uli, and the waste products of nitrogenous metabolism probably by the 
epithelium of the convoluted tubules. In disease the functional activity 
of the kidneys fails or becomes perverted, so that on the one hand, sub- 
stances normally eliminated are retained and accumulate in the blood, 
whereas, on the other hand, the kidney becomes pervious to substances 
that ordinarily do not pass it. This failure of excretion is in some way 
related to the predominating symptoms of nephritis — oliguria, uremia 
(in part, perhaps, retention of waste products of nitrogenous metabolism), 
and oedema (in part, retention of sodium chloride); and the abnormal 
permeability of the renal epithelium is answerable for the other significant 
manifestation of nephritis — albuminuria. The albumin discharged with 
the urine in disease is the albumin of the blood, serum albumin and 
globulin; this fact (and others) shows a selective action on the part of 
the cells of the glomeruli, which in health never excrete serum albumin, 
although they may excrete a foreign protein, such as egg-albumen, pep- 
tone, or the Bence-Jones albumose (myelopathic albumosuria), etc. Fur- 
thermore, although when diseased the kidney usually suffers as a whole, 
certain parts seem to be unduly susceptible to the action of certain 
poisons, as the glomeruli to the toxin of scarlatina — which provokes a 
so-called glomerulonephritis, especially characterized by oliguria. 

The urine, the totality of the excretory activity of the kidneys, is 
a measure not only of the functional capacity of the kidneys themselves, 
but also of other organs more or less remote from, though variously 
related to, the kidneys, and of the general metabolism. In diseased 



756 DISEASES OF THE URINARY SYSTEM 

conditions, then, the urine may exhibit (1) variations in its normal 
constituents, or (2) substances foreign to it in health (quantitatively or 
qualitatively); and these latter may be significant of (a) disease of 
the kidney and the urinary tract, or (b) disorders of general metabolism 
or of organs other than the kidney. 

Variations in the Normal Constituents of the Urine. — The 
total daily volume of the urine is a measure of the local renal and the gen- 
eral blood pressure, of the amount of blood circulating through the kidneys, 
and of the activity of the renal epithelium and of the skin. The reciprocal 
relations existing between the kidneys and the skin are of much im- 
portance in determining the amount of water in the urine: other things 
being equal, the more the sensible and insensible perspiration (activity 
of the skin) the less the water in the urine, and vice versa. In health the 
renal epithelium responds to the amount of blood that circulates through 
the kidneys : an increased amount of blood results in an increased amount 
of urine, and the reverse. Thus, for instance, when in consequence 
of cold, the cutaneous vessels become constricted and the kidneys (and 
other abdominal organs) receive an increased supply of blood, as well 
as when, in consequence of vasomotor relaxation (nervousness, fright), 
more blood is determined to the kidneys, the urine is increased. In 
acute inflammation, however, the increased amount of blood is associated 
with swelling and other degenerative changes of the renal epithelium, 
and, the renal capsule being comparatively inelastic, compression of 
the renal capillaries, slowing of the circulation, and consequent oliguria 
result. In these circumstances, the effect of heat (as opposed to cold) 
in determining blood to the cutaneous surface and reducing renal 
blood pressure is resorted to and constitutes the basis of valuable thera- 
peutic resources (flannel clothing, hot baths, warm climates, etc.). In 
these cases the administration of large amounts of water to flush the 
kidneys is neither wise nor efficacious, since before the kidneys can 
functionate properly the local circulatory conditions and the renal epi- 
thelium must become improved; for similar reasons, drugs that induce 
diuresis by increasing renal blood pressure are directly contra-indicated. 
The relief to tension is in part at least the rationale of decapsulation in 
subacute and chronic nephritis with oliguria. Oliguria results in all 
conditions of lowered renal blood pressure, as in chronic passive conges- 
tion, in shock, etc.; excretion ceases if the pressure is reduced to 40 mm. 
Hg. The polyuria of chronic indurative nephritis is due largely to 
increased general blood pressure — which is a manifestation of adaptation 
on the part of nature to compensate for changed conditions, and it should 
not, therefore, be too much reduced, since reduction may lead directly 
to oliguria and uremia. Polyuria also may be due to an effort on the 
part of the kidney to excrete a foreign substance such as sugar (diabetes), 
or to excrete the normal amount of normal ingredients when the kidneys 
become reduced in capacity (diabetes insipidus). 

The acidity of the urine is due to acid phosphates and organic acids. 
Special clinical importance attaches to /?-oxybutyric acid and its deriva- 



PATHOLOGICAL PHYSIOLOGY 757 

rives in the acidosis of diabetes and other conditions. The nitrog- 
enous constituents of the urine make up about 16 grams daily on an 
ordinary diet; about 85 per cent, is urea, 1 to 3 per cent, uric acid, 
2 to 5 per cent, ammonia compounds, and the remainder purin bases, 
creatinin, hippuric acid, etc. Of special clinical importance is the fact 
that the nitrogenous excretion in health is proportionate to the nitrog- 
enous intake; that it is futile to estimate the output of urea (formed 
largely in the liver from ammonia compounds) without at the same 
time estimating the total nitrogenous output and knowing the nitrog- 
enous intake (the protein content of the food); and that although the 
ratio of uric acid to urea is usually about 1 to 70, it varies considerably 
in health, depending upon the diet and other factors. The ammonia 
output has come to be recognized as a valuable measure of the presence 
or absence of acidosis, and is of much clinical importance in the acid 
intoxication of diabetes, pregnancy, etc. 

Chlorides, present chiefly as sodium chloride, are derived from the 
food, and in health the output is proportionate to the intake. In some 
cases of parenchymatous nephritis the renal epithelium appears to be 
incapable of excreting chlorides, which being retained constitute at least 
one factor in the causation of oedema. The phosphates also are derived 
largely from the food. The condition spoken of as phosphaturia is usually 
due not to excessive output, but to lessened acidity of the urine and pre- 
cipitation of earthy phosphates; rarely there may be an excessive output 
(so-called phosphatic diabetes) in neurasthenia, tuberculosis, diabetes, 
leukemia, etc. ; in some cases it seems to be associated with disturbances 
of the calcium metabolism. 

The sulphates result from decomposition of proteins, and occur as 
inorganic sulphates, ethereal (organic) sulphates, and neutral (unoxidized) 
sulphates. The ethereal sulphates result in part from metabolic pro- 
cesses, and in part from the union of sulphuric acid and certain aromatic 
products of intestinal putrefaction (phenol, indoxyl, skatoxyl); to some 
extent, then, they are a measure of intestinal putrefaction, and with 
reservation may be thus interpreted clinically (indicanuria). 

Oxalates (chiefly calcium) are derived largely from vegetable foods 
(spinach, rhubarb), but in part from metabolic processes. An increase, 
spoken of as oxaluria (sometimes spurious, due to precipitation in con- 
sequence of a poverty of magnesium salts), is sometimes associated with 
neurotic disorders, indigestion, etc.; and the salts sometimes constitute 
renal calculi. Urobilin is normally present in small amounts, and it is 
increased (urobilinuria) in cases of excessive erythrocyte destruction, 
(pernicious anemia, certain forms of hemolytic jaundice, etc.). 

Abnormal Constituents in the Urine. — Under varying circum- 
stances the urine contains a large number of substances foreign to it in 
health, quantitatively or qualitatively; of these, the most important are 
albumin, tube casts, blood, and pus — which are of much significance in 
the diagnosis of disease of the kidney and the urinary tract; furthermore, 
glycosuria and ketonuria (major phenomena of diabetes) also are common ; 



758 DISEASES OF THE URINARY SYSTEM 

and there are other more or less important anomalies of urinary excre- 
tion. 

Thus, the urine may be abnormally colored. Deep yellowish or orange- 
colored urine may be due to: an excess of urochrome (the normal 
urinary pigment); urobilin, due largely to the action of intestinal 
bacteria on bilirubin, and found in conditions of excessive hemolysis, 
pernicious anemia, hemolytic jaundice (sometimes inaptly called urobilin 
jaundice) constipation, etc.; uro-erythrin (liver disease, fevers, etc.); 
chrysophanic acid (rhubarb, senna); santonin, etc. Pinkish or reddish 
urine may be due to oxyhemoglobin (hemorrhage), uro erythrin (pinkish 
uratic sediment), eosin, rosanilin, etc. Greenish urine is due to the pres- 
ence of bile pigment (biliverdin) or methylene blue; bluish urine is 
practically always due to methylene blue. Brown or black urine may 
be due to methemaglobin (hemorrhage — which causes smoky urine; 
paroxysmal hemoglobinuria — so-called black-water fever); to an excess 
of bile pigment (especially biliverdin); to an excess of indican (blackness 
on standing; higher oxidation products of indol and not indoxyl sul- 
phate, which is colorless); to melanin or melanogen (disseminated 
melanotic tumors); to the ingestion of carbolic acid, creosote, salicyl 
compounds, etc.; to hematoporphyrin, which causes a port-wine or 
blackish discoloration of the urine as one of a series of toxic phenomena 
that occur especially in women after the long-continued use of sulphonal 
or trional, and perhaps under other circumstances (lead poisoning, intes- 
tinal hemorrhage) ; and to alkapton (alkaptonuria, a brownish or blackish 
discoloration of the urine upon exposure to the air, associated with 
reduction of Fehling's solution, but no other "sugar" reaction, no fer- 
mentation, and no rotation of polarized light) ; and ochronosis (blackish 
pigmentation of the cartilages), which is a congenital vice of metabolism 
(incomplete combustion of aromatic derivatives of proteins) , resulting in 
the presence in the urine of homogentisic acid; the linen may be stained 
black by the urine, and ultimately the cartilages of the ear, the sclerotics, 
and even the skin may become obviously pigmented. 

Other rare urinary anomalies comprise chyluria, which may be parasitic 
(true chyle) or non-parasitic — opaque, whitish, opalescent, milky urine; 
lipuria (fat in the urine), which may occur after an excess of fatty food, 
or of cod-liver oil, in fat embolism after fractures, in fatty degeneration, 
phosphorus poisoning, prolonged suppuration, diabetes, chronic nephritis 
with fatty degeneration, pyonephrosis, spurious chyluria, etc. ; choluria, 
the presence of bile pigments (bilirubin and biliverdin in cases of jaun- 
dice); cystinuria, of interest because rarely it may lead to the formation 
of cystin calculi; flbrinuria, the formation in the urine of a jelly-like 
mass, occasionally associated with marked albuminuria; pneumaturia 
(the presence of gas in the urine), which may result from trauma or 
the instrumental introduction of gas into the urinary tract, gas from the 
intestinal tract (vesico-enteric fistula), or fermentation of urine in the 
bladder by gas-forming organisms (Bacillus coli, Bacillus lactis aerogenes, 
Bacillus aerogenes capsulatus) — usually found in diabetic subjects. 



PATHOLOGICAL PHYSIOLOGY 759 

Uremia. — Uremia is a form of auto-intoxication that occurs in 
nephritis and in certain conditions associated with anuria. The toxic 
agent is not known. Commonly the uremic manifestations are ascribed 
to the activity of retained poisonous metabolic products that should be 
and in health are eliminated by the kidneys, and these products are often 
assumed to be nitrogenous in nature. The poison is not urea, uric acid, 
potassium or sodium salts, creatinin, etc., since these may be injected 
into the body without evil consequences. The condition has been attrib- 
uted also to an acid intoxication (lessened alkalinity of the blood), 
to urotoxins (Bouchard), to toxemia of the blood (Hughes and Carter), 
to oedema of the brain and meninges (Traube), to failure or perversion 
of a supposed internal secretion of the kidneys; to nephrolysins, etc. 
It is not improbable that it results from the products of perverted metab- 
olism or from non-detoxification of metabolic products normally robbed 
of the poisonous products (by the liver, for instance). The cerebrospinal 
fluid is often under increased pressure. 

Clinically uremia may be acute or chronic, or latent (in conditions 
of obstruction of the ureters and anuria). Acute uremia may occur 
in any type of nephritis, but it is especially common in acute and chronic 
diffuse non-indurative nephritis; it is often preceded by chronic mani- 
festations (headache, restlessness, dyspnoea, insomnia, etc.); it develops 
suddenly, is likely to last only a short time, and commonly leads to death. 
Chronic uremia is most common in chronic diffuse indurative nephritis; 
it develops insidiously, is mild in its manifestations, is likely to last a long 
time, may disappear and recur, but is likely ultimately to lead to acute 
manifestations and death. 

The major symptoms of acute uremia are nervous in nature and con- 
sist of (a) convulsions (not to be distinguished from those of epilepsy, 
except probably the absence of the initial cry); (b) coma, which, aside 
from that which attends and follows the convulsions, may come on insid- 
iously and last several days or weeks, and lead usually to death, but 
sometimes eventuates in recovery; and (c) psychic derangements (melan- 
cholia, delusional insanity, mania, etc.). Hemiplegia or monoplegia 
sometimes occurs, and may be due solely to oedema of the brain and 
meninges. Other less serious and more chronic nervous manifestations 
comprise headache, hemicrania, vertigo, insomnia, tinnitus aurium, am- 
aurosis, languor, neurasthenic phenomena, muscular pains and twitchings 
(especially in the calves), joint pains, etc. Dyspnoea (renal asthenia) is 
often an early and obtrusive sign; it may be continuous or paroxysmal 
(developing especially at night), or of the Cheyne-Stokes type. Nausea 
and vomiting (sometimes uncontrollable) are common, and may be asso- 
ciated with diarrhoea; these may result from toxic irritation of the medul- 
lary centres or from gastro-intestinal irritation provoked by the excretion 
of urea into the stomach and its decomposition into ammonia. Stomatitis, 
a coated tongue, and foul breath are frequent. The temperature is 
usually subnormal, although a so-called uremic fever has been described. 
Uremia is usually easily recognized, but in the event of coma one must 



760 DISEASES OF THE URINARY SYSTEM 

eliminate alcoholism (obvious alcoholism, alcoholic habits, less deep 
coma), opium poisoning (contracted pupils, infrequent respirations, no 
convulsions), diabetic coma (ketonuria, perhaps glycosuria, fruity odor to 
the breath, KussmauTs dyspnoea), and apoplexy (sudden onset of hemi- 
plegia, flapping of one cheek, conjugate deviation of the eyes, perhaps 
unequal pupils). Apoplexy, however, is common in chronic nephritic 
subjects, so that albumin and casts in the urine are not conclusive 
evidence of the one or the other condition; nor do they exclude diabetic 
coma, since at least one-half of the diabetic subjects have also chronic 
nephritis. 

Cardiovascular Changes in Nephritis. — The cardiovascular 
changes in nephritis are of extreme interest and importance; as a matter 
of fact, they dominate the clinical picture of the disease and they assume 
commanding position in the prognosis and in the treatment. The 
lesions are widespread, involving the heart, the large and the small 
arteries, the capillaries, sometimes even the veins. The lesions of the 
heart involve the muscle and find their expression in hypertrophy. With 
this, at times, there is associated some interstitial myocarditis, with 
increase of the intermuscular fibrous trabecular, especially in the neigh- 
borhood of many of the smaller coronary arteries, which frequently are 
obliterated. In some cases, especially late in the course of the disease, 
fatty degeneration of the heart muscle also may supervene. Valvular 
lesions are extremely uncommon. Those that are found in cases of renal 
disease are either an antecedent condition, or they result from mechanical 
causes, from dilatation of the heart, the lesion being one of relative 
insufficiency. The hypertrophy of the heart is predominantly a lesion of 
the left ventricle. In the majority of cases the left ventricle alone is 
affected; in the remainder of the cases both ventricles are affected. The 
right ventricle is never affected alone. Simple hypertrophy of the 
left ventricle is the first event; later, this is associated with some dila- 
tation — eccentric hypertrophy. The longer the nephritis continues (the 
longer the patient lives), the more certain the development of consecu- 
tive enlargement of the right ventricle, the increased pressure in the left 
ventricle, coupled with degenerative alterations in the heart muscle, 
leading to increased pressure in the right ventricle. Here also the hyper- 
trophy is of the eccentric variety. Predominating dilatation of either 
or both ventricles is an unusual event until toward the termination of 
life; its development is of ominous moment — it usually presages an early 
fatal termination. It has been stated by Senator and others that the 
hypertrophy of the primarily contracted kidney is of the simple variety, 
whereas that associated with the secondarily contracted kidney and with 
the arteriosclerotic kidney is of the eccentric variety — hypertrophy with 
dilatation. But this statement scarcely permits of general application. 

This hypertrophy of the heart occurs in all forms of nephritis, but not 
in all cases. In none of the varieties, however, does it so dominate the 
clinical picture as it does in chronic indurative or interstitial nephritis. 
It may be expected from the time of the contraction or atrophy of the 



PATHOLOGICAL PHYSIOLOGY 761 

kidney, be it of the primary or the secondary variety. Thus it occurs 
early in the primary form, but its occurrence may be (but usually is not) 
much delayed in the secondary form. It may, however, occur in chronic 
diffuse non-indurative (or parenchymatous) nephritis, and it is observed 
in some cases of acute nephritis, particularly in some of the cases of 
acute nephritis following the infections. In some of the chronic cases 
in which it should be expected, for some more or less inexplicable reason 
it may not occur, at all events not to a noteworthy degree. These, how- 
ever, are the unusual cases. The absence of the hypertrophy may be 
due to faulty nutrition — the heart not being sufficiently well nourished 
to enable it to hypertrophy; to sclerosis of the coronary arteries; to the 
vicarious action of one of the other emunctories removing those excre- 
mentitious products ordinarily eliminated by the healthy kidneys, etc. 

The changes in the arteries are those of augmented blood pressure, 
and arteriosclerosis and atheroma. These changes, though widespread, 
are not distributed uniformly throughout the body. In many cases they 
are most marked in the kidneys; in a few cases they appear to be almost 
confined to them. In many cases small miliary aneurysms develop, 
especially in the brain, and rupturing, frequently lead to the fatal ter- 
mination. 

The cause of these cardiovascular alterations has not been thoroughly 
worked out. Considerable discussion still obtains with reference to 
whether the primary alterations are in the arterioles (stopcock action of 
Johnson) or in the capillaries (the arteriocapillary fibrosis of Gull and 
Sutton). Doubtless, the conditions differ in different cases. Thus, 
arteriosclerosis itself may be the primary event (and this seems to be 
especially common in this country), and it leads to both the kidney 
alterations and the cardiac hypertrophy. In this instance the disease 
is a widespread process, and its etiology is the etiology of arteriosclerosis. 
However, in many cases the nephritis is the primary event, and leads 
to the cardiovascular alterations. Whether these are mechanical or 
chemical in nature is still a matter of discussion. Augmented blood 
pressure is undoubtedly at the bottom of the process, but the old view 
of Traube and of Cohnheim that this resulted from an effort on the part 
of the cardiovascular system to maintain a normal or adequate flow of 
blood through kidneys, the capillary distribution of which had become 
reduced by interstitial overgrowth, has been largely given up. It has 
been modified to some extent by certain observers, who point out that 
these cardiovascular lesions occur most commonly in association with 
disease of the glomeruli, and that the function of the glomeruli seems to 
be that of filtration dependent upon the blood pressure (as contrasted 
with the glandular secretory activity of the renal epithelium); and they 
suggest that when the glomeruli become more or less inactive in conse- 
quence of disease, the regulatory mechanism of the body attempts to 
compensate therefor (to promote glomerular elimination) by increased 
blood pressure — which becomes general. On the other hand, it has 
been suggested that the primary increase of blood pressure is chemical 



762 DISEASES OF THE URINARY SYSTEM 

in origin, is due to the angiotonic properties of the adrenal body; that 
the condition results from hyperadrenalism. Alterations, interpreted by 
some observers as hyperplastic in nature, have been found in the 
adrenals in nephritis (although it has not yet been determined whether 
they are the cause or the result), and a pressor substance has been found 
in the disordered kidneys. Whether this is adrenalin or a substance 
allied thereto, and whether this is the result of increased formation or 
of retention (reduced elimination by diseased kidneys), has not been 
determined. Perhaps certain enterogenic or other poisons not detoxi- 
fied by the liver may be at the bottom of the process. 

The Functional Capacity of the Kidneys. — The most obvious 
is at the same time the best test of the functional capacity of the kidneys 
— the daily amount of the urine; for suppression of urine is a certain 
sign of renal inadequacy (whether the primary cause be resident in the 
kidneys themselves or elsewhere, such as the cardiovascular system). In 
addition to oliguria or anuria, albuminuria, cylinduria, and uremia are 
important manifestations of functional incapacity of the kidneys; these 
are discussed under separate headings. 

Other tests of the functional capacity of the kidneys comprise: (1) 
The indigo-carmine test. This consists of the intramuscular injection 
(gluteal muscles) of 20 c.c. of a 0.4 per cent, aqueous solution of indigo- 
carmine, and ascertaining, preferably by means of cystoscopy, the time 
of beginning excretion (light blue color to the urine) and the time of 
maximum excretion (dark blue color) of the indigo-carmine. Normally 
the excretion begins within twenty minutes (averaging perhaps fifteen) ; 
if the excretion is delayed beyond twenty minutes, certainly if beyond 
thirty minutes, serious or grave disease of the kidneys is almost certain. 
This test is especially significant of surgical diseases of the kidney or 
obstruction of the ureter. (2) The methylene blue test. This com- 
prises the intramuscular injection of 1 c.c. of a 5 per cent, aqueous 
solution of methylene blue; the collection of the urine after the lapse 
of one-half hour, one hour, and hourly thereafter; and noting the time 
of the appeareance of a bluish tint to the urine, the time of maximum 
coloration, and the time of disappearance of the coloring. Normally a 
slight tint may be noticed in the first specimen, certainly at the end 
of one hour; the maximum coloration occurs at the end of three or four 
hours, and the urine is free of coloring at the end of thirty-six to 
forty-eight or sixty hours. Delay of beginning excretion beyond one 
hour and of maximum coloration beyond the fourth hour, and con- 
tinuation of excretion, as may occur for five or six days, is indicative 
of deficient functional capacity. (3) The phloridzin (glycosuric) test. 
This consists of the intramuscular injection of 1 c.c. of a 0.5 per 
cent, aqueous solution of phloridzin, and the collection of the urine as 
in the methylene blue test. In normal subjects glycosuria may be de- 
tected at the end of one-half to one hour, and it disappears at the end 
of two to four hours. In disordered renal epithelium this glycosuria 
may be delayed or may not occur at all. (4) Cryoscopy, or the deter- 



ANURIA 763 

mining of the freezing point of the urine, is a test of its molecular con- 
centration, particularly of its sodium chloride ions and protein con- 
stituents. Normally, the freezing point of the urine varies between 
— 1.3° and — 2.3° C; in diseased states the freezing point is — 1° or less 
than — 1° C. (hyposthenuria), but since this depends upon various 
factors (sodium chloride, protein constituents, urates, etc.) it loses 
clinical value. Comparison of the freezing point of the urine with 
that of the blood, which normally is — 0.56° C, is of more value. (5) 
The electrical conductivity of the urine. This varies with the contained 
ions, but is influenced by molecules that do not dissociate (sugar, etc), 
so than its clinical value is slight. All of these tests are of more value 
in determining the relative functional capacity of the two kidneys (sepa- 
rated urines) than the absolute functional capacity of both kidneys 
together, and they are especially applicable in surgical conditions of 
the kidneys and ureters. 

ANURIA. 

Anuria, or suppression of urine, in which no urine enters the bladder, 
should be distinguished from retention of urine, in which urine, though 
present in the bladder, is not or cannot be voided. In retention (unless 
as in typhoid fever, for instance, the sensibility is benumbed) there is 
likely to be complaint of distress referred to the bladder, although in 
some of the cases, such as elderly men with enlarged prostates, some 
overflow of urine may be associated with extraordinary retention of 
residual origin altogether unknown to the patient; in any event, how- 
ever, examination of the bladder region and catheterization will reveal 
the presence or absence of urine in the bladder. The causes of reten- 
tion are some mechanical obstruction (urethral stricture or stone, 
enlarged prostate, pregnant uterus, etc.) or some functional incapacity 
(paresis from overdistention, functional and organic diseases of the 
nervous system, etc.). Anuria may be obstructive or non-obstructive. 

Obstructive Anuria. — Obstructive anuria results- from compression of 
both ureters, as by a pelvic growth, such as a uterine carcinoma, for 
instance; blocking of both ureters by renal calculi, blood clots, tuber- 
culous material, tumors, twists or stricture, etc.; or blocking of one ureter 
in cases in which the other kidney is absent or functionless. The anuria 
in these cases, which are sometimes spoken of as " latent uremia," may 
persist for some time (one or two weeks or, rarely, longer) and the 
patient suffer comparatively little discomfort. Uremia (convulsions, 
coma, or psychoses) and oedema are quite unusual. The treatment is 
surgical. 

Non-obstructive Anuria. — Non-obstructive anuria occurs: (1) In acute 
toxic degenerative and diffuse nephritis, such as occurs in the infective 
diseases (scarlet fever, yellow fever, cholera, etc.) and in different poi- 
sonings (phosphorus, lead, cantharides, etc.); (2) in cardiovascular 
failure, and passive congestion; (3) following severe, especially abdom- 



764 DISEASES OF THE URINARY SYSTEM 

inal injuries and operations (sometimes even the passing of a catheter), 
particularly in persons past middle life whose kidneys and bloodvessels 
are somewhat damaged; and (4) as a manifestation of hysteria (although 
hysterical retention and deception are more common). Aside from 
hysterical anuria, in which, as in obstructive anuria, there is usually 
a remarkable absence of symptoms, non-obstructive anuria is of serious 
moment — being one of the manifestations of serious degeneration of the 
kidney or nephritis. The treatment is that appropriate in acute diffuse 
nephritis. 

ALBUMINURIA. 

Albuminuria is a term used to denote the presence in the urine of 
different protein substances — serum albumin, serum globulin, nucleo- 
albumin, album ose, peptone, fibrin, and hemoglobin. While formerly 
regarded as diagnostic of Bright's disease, albuminuria is now known to 
be dependent upon many different diseased conditions. Large amounts 
of albumin in the urine, however, practically always indicate serious 
kidney disease, but serious disease of the kidneys may exist for a long 
time with little or no albumin in the urine. In the majority of cases 
of albuminuria the albumin is moderate in amount, and one generally 
has to determine whether the albumin is due to disease of the kidneys, to 
disease of some other organ, or to both. The importance and significance 
of albuminuria are always enhanced by the associated presence of tube 
casts, but both albumin and casts may be present without serious disease 
of the kidneys, and serious forms of Bright's disease may exist with 
at least temporary absence of albumin and casts from the urine. The 
differential diagnosis of albuminuria, therefore, is of considerable 
importance. The following forms of albuminuria may be distinguished : 
(1) Extrarenal, spurious, accidental, or factitious albuminuria; (2) 
so-called functional, physiological, or cyclic albuminuria; (3) albuminuria 
without noteworthy alterations in the kidneys; and (4) albuminuria 
with noteworthy alterations in the kidneys. 

Extrarenal, Spurious, Accidental, or Factitious Albuminuria. — In these 
cases the albuminuria is but a subsidiary factor and entirely dependent 
on the admixture with the urine of different albuminous fluids — blood, 
pus, chyle, or seminal discharges. Chyle is a very rare constituent of 
the urine, and when present will scarcely fail of recognition. Seminal 
discharges in the urine are of more common occurrence, and should not 
escape careful observation. The greatest interest attaches to cases of 
albuminuria associated with blood and pus in the urine — the result of 
inflammation and ulceration of, and of hemorrhage from, any part of the 
genito-urinary tract, especially the renal pelvis, ureters, bladder, urethra, 
vagina, uterus. In these cases the amount of albumin is small — rarely 
more than 1 part per 1000 (Esbach's method), and it is proportionate 
to the amount of blood and pus. A disproportionate amount of albu- 
min should always excite a suspicion of the co-existence of nephritis. 



ALBUMINURIA 765 

The presence of tube casts in the urinary sediment is of the great- 
est importance — their persistence being clear evidence of nephritis, 
and indicating that at least a part of the albumin in the urine is due 
to circulatory and tissue changes in the kidneys. One must avoid 
error in presuming the non-existence of nephritis in cases in which a 
small amount of albumin and casts are associated with a few leukocytes 
or pus corpuscles. In most of these cases the albuminuria is due in 
great part to nephritis — a few leukocytes or pus corpuscles being regular 
constituents of the urine in Bright's disease. (For additional informa- 
tion, see hematuria, pyuria, and nephritis.) 

So-called Functional, Physiological, Cyclic, Intermittent, Paroxysmal, 
Dietetic, Postural (Orthostatic), and Adolescent Albuminuria. — The occur- 
rence of a " physiological" albuminuria is now generally conceded. It 
is found especially in young, more particularly male, subjects under 
twenty-five years of age. It is usually detected accidentally, as, for 
instance, at examinations for life insurance, or for other certificates of 
health. In some cases it appears to be constant, and it lasts for a relatively 
long time; in other cases it is intermittent — occurring at stated or inde- 
terminate periods. In many of the cases the presence and the amount 
of the albumin are much influenced by certain circumstances — posture 
(whence it is sometimes absent on arising in the morning and present 
later in the day), exercise, emotional and other excitement, cold baths, 
certain articles of diet (especially proteins, but also large amounts 
of ordinary mixed foods), prolonged anxiety, college and university 
examinations, etc. In diagnosticating this form of albuminuria consider- 
able circumspection must be exercised. The patient should be a young 
subject; the urine should be normal in amount (certainly not increased), 
normal in color, and normal in specific gravity (certainly not of lessened 
specific gravity); the amount of albumin must be small — less than 0.5 
per 1000 (Esbach); the urine must contain no other abnormal constit- 
uent; there must be no local disease of the genito-urinary tract, such as 
gleet, spermatorrhea, leucorrhea, etc., that might give rise to spurious 
albuminuria; every bodily organ must be examined and found to be in 
perfect health — in particular there must be no hypertrophy of the left 
ventricle of the heart, no accentuation of the aortic second sound, and 
no increased arterial tension; nor may there be any evidence of disorder 
of the heart, lungs, or liver that might occasion congestion of the kidneys; 
there must have been no past, nor may there be any present, oedema, 
uremic manifestations, or retinal changes; and at the most there must 
not be more than an occasional hyaline cast. Even in cases that meet 
these requirements much caution must be observed, and the diagnosis 
must not be made until the patient has been long under observation, 
until both the morning and the evening urines have been repeatedly 
examined, and until the albumin is found to vary with the influences 
under which it develops. And when the diagnosis has been made one 
should stand willing to renounce it immediately on the development 
of signs of disease likely to be attended by albuminuria. Caution is 



766 DISEASES OF THE URINARY SYSTEM 

always necessary, inasmuch as albumin may be temporarily absent, 
even for long periods in certain cases and at certain stages of chronic 
indurative (or interstitial) nephritis, whereas, in other cases it may be 
present in such small amounts as to require delicate tests for its detec- 
tion. More than a small amount of albumin always suggests a latent 
nephritis that for the time being may reveal itself by no sign other than 
the albuminuria. The caution necessary in the diagnosis of these cases 
is evident from the statement of Senator, who believes that most cases 
of so-called cyclic or functional albuminuria are really cases of latent 
nephritis, and that no case of albuminuria may be regarded as functional 
or physiological if the albumin exceeds 0.4 or 0.5 part in 1000. The 
diagnosis of functional albuminuria in late adult life had best be dis- 
pensed with entirely, as practically without exception small amounts of 
albumin in the urine of such subjects means chronic nephritis (excluding 
cases of extrarenal albuminuria). 

The cause of this functional or cyclic albuminuria is not well understood. 
It has been attributed to vascular alterations (congestion) of the kidneys, 
and to disturbances in metabolism, in consequence of which albumoses, 
excessive in quantity or abnormal in quality, are formed. That many 
of these cases are really cases of physiological albuminuria may well be 
doubted. Some of them are certainly cases of spurious albuminuria. 
In most cases it is likely that the glomerular epithelium suffers some 
nutritional disturbance. In some cases the renal epithelium is probably 
unduly sensitive. These cases may be confounded with the rather un- 
usual cases in which following an acute nephritis in early childhood a 
trace of albumin persists throughout life, but the patient lives to a good 
old age without other manifestations of nephritis developing. Such per- 
sistent albuminuria, of course, indicates slight alterations in the renal 
epithelium, and in case careful injuiry is not made into the antecedent 
history of the patient the condition may be regarded as "physiological" 
albuminuria. 

Albuminuria without Noteworthy Alterations in the Kidneys. — A slight 
amount of albumin may be found in the urine in a great variety of morbid 
conditions without noteworthy alterations in the kidneys. Thus it may 
be found in different blood conditions, such as the anemias, leukemia, 
purpura, scurvy, etc.; in certain forms of intoxication, such as lead 
poisoning, mercurial poisoning, etc.; in conditions associated with the 
presence of substances, such as sugar and bile-pigment in the blood; 
after the administration of anesthetics; in fever conditions, and in certain 
nervous disorders — epilepsy, apoplexy, meningitis, tetanus, exophthalmic 
goitre, injuries to the head, etc. In most of these cases the albuminuria 
is attributable to nutritional disturbances in the glomeruli and renal 
epithelium induced by defective blood supply; in some cases to the result 
of nervous influences. The true nature of these cases is usually readily 
recognized. The albuminuria is slight and temporary, as a rule; the 
primary disorder is sufficiently obvious, and there is no other manifesta- 
tion of Bright's disease. It is important, however, to point out that the 



ALBUMOSURIA 767 

conditions in the kidneys found in some of the intoxications and in 
fever states (toxic degeneration of the renal epithelium) merge gradually 
into the well-defined lesions of nephritis — that there is no sharp divid- 
ing line between them. 

Albuminuria with Noteworthy Alterations in the Kidneys. — In this group 
are included the cases of active and passive congestion of the kidneys, 
cases of toxic degeneration of the kidneys (most of the cases of febrile 
albuminuria), the kidney of pregnancy, amyloid degeneration of the 
kidneys, the acute and chronic suppurative and non-suppurative inflam- 
mations of the kidneys, and tumors of the kidneys. In all of these cases 
the albuminuria is due to some more or less severe, temporary or perma- 
nent, damage to the kidneys, and the albuminuria acquires its clinical 
significance and diagnostic importance from the attendant phenom- 
ena. In acute congestion of the kidneys the albumin is small in amount, 
the urine is decreased in quantity and frequently more or less hemor- 
rhagic, and the causative factor usually can be determined. In most 
cases, however, acute congestion of the kidneys represents but the early 
stage of acute nephritis, from which it is scarcely to be differentiated. 
In chronic congestion the albumin varies in amount in different cases. 
In chronic heart and lung diseases it is usually small in amount, but in 
cases of chronic congestion due to obstruction of the renal veins by a 
tumor or ascites, etc., the amount may be large. The diagnosis of 
chronic congestion is to be based on the attendant phenomena and not 
on the amount of albumin. Toxic or febrile albuminuria is an interesting 
condition that merits much attention. The albumin in these cases is due 
to the direct action of some toxin on the renal epithelium rather than to the 
fever, though this may be a contributing factor; in the one case the 
toxin induces marked degeneration of the renal epithelium, in another 
case it leads to severer lesions — to an acute nephritis. In toxic albumin- 
uria the albumin is slight or moderate in amount and transitory, dis- 
appearing with the intoxication or infection that gives rise to it. 

ALBUMOSURIA. 

True albumose is sometimes found in the urine — during postpartum 
involution of the uterus (physiological), during fevers, during absorption 
of pneumonic exudates, in phosphorus poisoning, in acute yellow atrophy 
of the liver, and in other conditions of autolysis — to which it is attrib- 
utable. True peptonuria has occasionally been found in pneumonia, 
tuberculosis, etc. Globulin is occasionally found in association with large 
amounts of albumin; it may occur alone. 

The Bence-Jones protein (myelopathic albumosuria; Kahler's dis- 
ease) is a protein foreign to the blood in health; it is formed in multiple 
myeloma, of which it is diagnostic; and it may be excreted by normal 
kidneys without impairment of their epithelium (selective action). 
It is distinguishable from ordinary albuminuria by the production of 
cloudiness in the urine when heated to 50° C, by a flocculent precipitate 



768 DISEASES OF THE URINARY SYSTEM 

between 50° and 60° C, by solution of the precipitate at higher temper- 
atures (especially upon the addition of acetic acid), and by reprecipita- 
tion upon cooling. 

CYLINDRURIA. 

The term cylindruria is commonly employed to designate casts of 
the uriniferous tubules (cylinders, tube casts), although perhaps other 
casts might be included within the scope of its meaning; these, how- 
ever are casts of the renal pelvis, ureter, urethra, etc., and since they 
are usually made up of blood, they are referred to under hematuria. 
Tube casts basically are made up of coagulated serum or a serum- 
like substance exuded by the renal epithelium when irritated, or perhaps 
they result from the interaction of serum and another substance elabo- 
rated or liberated by disordered renal epithelium. The basic (hyaline) 
cast may become altered or attach various sorts of cells, and debris, 
so that different kinds of casts may be distinguished — hyaline, waxy, 
granular (pale and dark), and cellular; of the cellular casts, some- 
times (but by no means always) the type of cell may be distinguished 
— epithelial, leukocytic, erythrocytic; an obvious fatty degeneration of 
the cells, as well as free fat droplets, suggests the term fatty cast; and 
some casts apparently consist wholly of leukocytes or erythrocytes 
without the basic hyaline material. 

Considerable diagnostic significance attaches to the presence of casts. 
They suggest mere irritation (hyaline cast) or more complete destruction 
and desquamation of the renal cells (epithelial, granular, and fatty casts). 
A few hyaline casts may occur in conditions of slight nutritive disturb- 
ance, such as occurs in congestion; and since the renal epithelium is not 
markedly disturbed in chronic interstitial nephritis, few casts are encoun- 
tered. Many, especially epithelial and granular, casts indicate marked 
alteration and desquamation of the renal epithelium, such as occur in 
parenchymatous nephritis. Casts and albumin may and usually do occur 
together, but either may occur alone; casts alone are the more significant 
of changes in the renal epithelium. Few casts for a short time signify 
a mere transitory disturbance; the continued presence of even a few 
casts means chronic nephritis; many cellular (epithelial) casts mean 
serious parenchymatous involvement of the renal epithelium; erythro- 
cytic casts, an acute exacerbation; and a lessening number of cellular 
and erythrocytic casts, a subsiding process, etc. 

Too much importance must not be attached to a few hyaline or cellu- 
lar casts in a single specimen of urine; they are common in transitory 
conditions, such as anemia, various intoxications, certain infections, etc., 
and although they indicate some disturbance in the renal epithelium, they 
subside with the initiating cause : the renal condition is not nephritis, as 
is too often supposed, and the kidney often becomes entirely normal 
again. Casts should not be mistaken for pseudocasts or cylindroids — 
long hyaline or longitudinally striated objects with undulating outline and 
tapering ends; these are mucoid in nature and not related to true casts. 



PYURIA 769 



HEMATURIA. 

Blood in the urine may come from any part of the genito-urinary tract. 
Care must be exercised to exclude menstrual blood and urine stained 
with logwood, rhubarb, etc. . Small amounts of blood in the urine may 
escape naked-eye observation; moderate or large amounts impart a dark 
brownish or smoky color; while very large amounts may appear as bright 
or dark red blood. The blood may be recognized by microscopic, 
spectroscopic, or chemical examination. 

Etiology. — Hematuria may be due to: (1) Disease of the urethra — 
usually traumatic (catheterization, bougieing, passing of a calculus, etc.), 
of which there is a history. The blood is pure and unmixed, and escap- 
ing at any time may stain the patient's linen. (2) Disease of the pros- 
tate — benign or malignant enlargement, of which hematuria is some- 
times one of the earliest manifestations. (3) Disease of the bladder — 
calculus, tumor (benign or malignant), ulceration (simple or tuber- 
culous), parasites, foreign bodies, varicose veins, etc. Blood from the 
bladder is usually quite apparent, not intimately mixed with the urine, 
often irregularly clotted, and may escape at the end of micturition; 
bladder epithelium and blood corpuscles are detected by microscopic 
examination (hemoglobinuria does not occur alone); irrigating the 
bladder results in securing a blood-tinged fluid; and the local symptoms 
are referred to the region of the bladder. (4) Disease of the kidneys — 
chronic congestion (heart disease); acute and chronic nephritic; infarc- 
tion; tumor formation; tuberculosis; calculus; parasitic invasion; etc. 
Blood from the kidney is often not immediately apparent (the urine being 
smoky only); it is usually intimately mixed with the urine (although 
there may be clots partaking of the shape of the pelvis or the ureter); 
blood casts, renal and pelvic epithelium are usually found in the sedi- 
ment, and blood corpuscles may be missed (that is, hemoglobinuria may 
occur alone); irrigating the bladder results in securing a clear fluid; 
and local symptoms are usually referred to the region of the kidney or 
the testicles. Cystoscopic examination and catheterization of the ureters 
also may be of value in differentiating vesical and renal hematuria. 
The association of pus and blood is significant of disease of the pelvis 
rather than of the renal substance. (5) Certain general disorders, such 
as hemophilia, scurvy, leukemia, and certain specific infective dis- 
eases, etc. 

PYURIA. 

Pyuria, or pus in the urine, may be due to suppuration of any part 
of the genito-urinary tract, or rarely to the rupture of an abscess (pelvic, 
prostatic, peri-appendicular, etc.) into the urinary tract. Pus occasions a 
general cloudiness of the urine, and a whitish or cream-colored, ropy, 
or tenacious sediment, which may be distinguished from a somewhat 
49 



770 DISEASES OF THE URINARY SYSTEM 

similar deposit of phosphates by the fact that the phosphates are whiter, 
less dense, and are decomposed by the addition of an acid. Microscopic 
examination completes the differentiation. 

Etiology. — Pyuria may be due to: (1) Disease of the urethra — usually 
urethritis, rarely a chancre. The pus is small in amount, escapes with 
the urine first voided, as well as between micturition, and is associated 
with painful micturition, other signs of local inflammation, and the 
presence of the gonococcus. (2) Vaginitis, in which in addition to 
evidences of local inflammation, vaginal epithelium and possibly the 
gonococcus may be encountered. (3) Cystitis, in which the urine may 
be acid when voided (Bacterium coli infections), but is usually or soon 
becomes alkaline (Proteus vulgaris, streptococcic, staphylococcic, and 
other infections), and is associated with triple phosphates, bladder 
epithelium, an ammoniacal odor, and other evidences of decomposi- 
tion. (4) Ureteritis, which is difficult (in many cases impossible) to 
differentiate from pyelitis, except by evidences of local inflammation. 
(5) Pyelitis and pyelonephritis. The pus is usually considerable in 
amount and associated with renal and pelvic epithelium, and in 
pyelonephritis may escape intermittently; the urine is usually acid in 
reaction (calculous disease, Bacillus tuberculosis and Bacterium coli 
infections, etc.), but if the pyelitis is secondary to cystitis the urine may 
be alkaline. 



ANOMALIES OF FORM AND POSITION OF THE KIDNEY. 

The kidneys are subject to several malformations and malpositions 
of clinical interest. One or both kidneys may be absent; one may be 
hypoplastic and the other hyperplastic; there may be a supernumerary 
kidney; and the two kidneys may be fused — horseshoe kidney, disk- 
shaped kidney. 

There may also be anomalous ureters (double or triple — unilateral 
or bilateral), and anomalous bloodvessels (of etiological significance 
in hydronephrosis). These anomalies acquire clinical interest in con- 
nection with contemplated operations on the kidney; the presence and 
the functional capacity of its fellow should always be determined before 
an operation on a kidney is undertaken, especially an operation that 
may comprise removal of the organ. The malpositions of the kidney 
(movable kidney, floating kidney, nephroptosis) are discussed in con- 
nection with visceroptosis (page 685). 



CIRCULATORY DISTURBANCES OF THE KIDNEYS. 

Active Congestion. — Active (acute) congestion is rare without con- 
current exudation; that is, there is no sharp dividing line between acute 
congestion and acute nephritis. Acute congestion has been attributed 



CIRCULATORY DISTURBANCES OF THE KIDNEYS 771 

to sudden contraction of the peripheral bloodvessels induced by exposure 
to cold, and to increased functional activity, such as may occur in one 
kidney if the ureter of its fellow be blocked by calculus, clot, etc., or if 
the organ itself be removed. Otherwise the causes of acute congestion 
are the causes of acute nephritis. The lesions, except in that they dis- 
appear with removal of the exciting cause, are not distinguishable from 
those of the mild grades of acute toxic or degenerative nephritis. 

Passive Congestion. — Passive (chronic or mechanical) congestion of 
the kidneys is usually part of the general venous stasis that accompanies 
chronic cardiac disease (myocardial, endocardial, or pericardial) ; it may 
occur also in the event of obstruction to the return circulation from the 
renal veins by pressure (tumor, aortic aneurysm, pregnant uterus, ascites), 
angulation (nephroptosis, kyphosis, etc.), or thrombosis or embolism of 
the renal vein or veins or the ascending vena cava. The kidney is enlarged 
and firm; the capsule strips readily and reveals distended veins and a 
smooth, dark bluish-red surface. The cortex is increased in thickness; 
the pyramids are purplish. In the course of time the organ may lessen 
in size, the capsule become slightly adherent, and the surface somewhat 
granular, due to the gradual growth and subsequent contraction of fibrous 
connective tissue and consecutive destruction of the parenchyma (the 
congested and contracted kidney; cyanotic induration). The symptoms 
consist of oliguria (retarded circulation of the blood and lessened arterial 
pressure) — perhaps 200 c.c. or less in the twenty-four hours; the urine 
is high colored, turbid, of increased specific gravity (1022 to 1035), 
deposits a considerable sediment of uric acid and urates, contains a 
small amount of albumin (usually less than 2 parts per 1000, Esbach's 
test), a few hyaline (rarely cellular) casts, and a few leukocytes and 
erythrocytes. The diagnosis is easy, being based upon a recognition of 
the primary disorder; other evidences of general venous stasis (enlarge- 
ment of the liver and spleen, oedema, dropsy, etc.), or a local factor 
obstructing the renal return flow; the urinary findings ; and fluctuation 
of the oliguria and albuminuria with the functional activity of the car- 
diovascular system. The cyanosis and dropsy contrast strongly with the 
pallor and dropsy of nephritis. The prognosis and treatment are those 
of the primary disorder. 

Thrombosis and Embolism. — Primary thrombosis is very rare; 
embolism is more common, and is due usually to left-sided endocar- 
ditis. The lesions consist of the common wedge-shaped anemic infarcts 
— which may be simple and ultimately replaced by a contracted scar, 
or infected and give rise to abscesses. The symptoms often are not 
obtrusive; but the diagnosis may sometimes be made upon the sudden 
onset of severe pain in the region of the kidney (without radiation down 
the ureters — which distinguishes it from renal colic); enlargement and 
tenderness of the kidney; oliguria, hematuria, and albuminuria of sudden 
onset and often of rapid disappearance; and in the event of the embolus 
being infected, chills, fever, sweats, leukocytosis (which, however, may 
be already present in consequence of the primary infection). 



772 DISEASES OF THE URINARY SYSTEM 



NEPHRITIS. 

The following varieties of inflammation of the kidneys may be dif- 
ferentiated : 

I. Acute nephritis. 

(a) Acute toxic or degenerative nephritis. (Cloudy swelling 

or parenchymatous degeneration of the kidney.) 
(6) Acute diffuse nephritis. (Acute parenchymatous, exuda- 
tive, catarrhal, desquamative, glomerular, tubular, or 
hemorrhagic nephritis.) 

(c) Acute suppurative nephritis. 

(d) Acute interstitial non-suppurative nephritis. 

(e) The kidney of pregnancy. 
II. Chronic nephritis. 

(a) Chronic diffuse non-indurative nephritis. (Subacute and 
chronic parenchymatous, exudative, catarrhal, desquama- 
tive, glomerular, tubular, or hemorrhagic* nephritis; the 
large white kidney; the large red, mottled, or variegated 
kidney.) 

(6) Chronic diffuse indurative nephritis. 

1. Secondary chronic indurative (or interstitial) nephritis. 

(Late stage of chronic parenchymatous nephritis; the 
small white kidney; the white granular kidney; the 
secondarily contracted kidney.) 

2. Primary chronic indurative (or interstitial) nephritis. 

(The red granular kidney; the gouty kidney; the pri- 
marily contracted kidney; the genuine contracted 
kidney.) 

3. Arteriosclerotic nephritis. (The senile kidney.) 
Strictly speaking, the so-called toxic or degenerative nephritis is not 

a true inflammation; but it is due to factors which if prolonged or of 
increased virulence result in inflammation, it is often associated with 
more or less active congestion and slight exudation, and it is the impor- 
tant lesion in well-developed acute nephritis, so that it is not only wise 
to include it among the acute nephritides, but practically it is virtually 
impossible to exclude it therefrom : it represents an early stage, a minor 
grade, or a part of acute nephritis. Acute suppurative nephritis will be 
discussed under a special heading; acute interstitial non-suppurative 
nephritis is largely of pathological, of little clinical, interest; the kidney 
of pregnancy is a peculiar type of obvious etiological relationships. 

Practically, therefore, in the great majority of acute cases the physician 
has to deal with what may be best described as acute diffuse nephritis, or 
simply acute nephritis ; or with an acute exacerbation of chronic nephritis. 
The chronic nephritides can be sharply divided into: (1) Those that 
follow subsidence of the acute process, or perhaps begin subacutely or 
insidiously, and are characterized by predominant, but not exclusive 



ACUTE DIFFUSE NEPHRITIS 773 

changes in the parenchyma (chronic diffuse non-indurative, or paren- 
chymatous, nephritis) ; and (2) those in which the chief lesions occur 
in the interstitial tissue (chronic diffuse indurative, or interstitial, neph- 
ritis), but in which the renal lesions, diagnostically, prognostically, and 
therapeutically, may be neither primary nor of the greatest importance 
(cardiovascular-renal disease). The chronic diffuse, non-indurative, or 
parenchymatous nephritis is often subject to acute exacerbations, and 
should the patient survive for eighteen months or more, sclerotic or 
cicatricial lesions may develop, and a form of so-called mixed nephritis 
(secondarily contracted kidney) may ensue. 



ACUTE DIFFUSE NEPHRITIS. 

(Acute Parenchymatous Nephritis; Acute Bright's Disease.) 

Etiology. — Acute nephritis may occur at any age, but is most common 
before the fortieth year and in males (excluding the kidney of pregnancy). 
Rarely it seems to follow directly upon exposure to inclemencies of the 
weather, especially coldness and dampness (said to cause reflex con- 
gestion of the kidneys, to favor the retention of excrementitious sub- 
stances, to produce a hemolysin analogous to that which occurs in 
certain cases of paroxysmal hemoglobinuria, etc.); these cases usually 
occur in alcoholic subjects. Otherwise, acute nephritis is due to autog- 
enous or exogenous infection or intoxication, and it is commonly a 
secondary process. The infectious causes comprise the infectious dis- 
eases, especially scarlatina, diphtheria, pneumonia, typhoid fever, influ- 
enza, cholera, yellow fever, smallpox, the pyococcic infections, etc. In 
most of these cases the renal lesions are due to toxemia and the excretion 
of toxins, rather than to bacteremia; the bacteremia of septicopyemia is 
likely to result in suppurative lesions (suppurative nephritis). The 
etiological intoxications comprise (in addition to the toxemias of the 
infectious processes) : (1) Autogenous metabolic poisons, associated with 
pregnancy, anemia, gout, diabetes, jaundice, hemoglobinemia, burns, 
diseases of the skin associated with lessening of the cutaneous functions, 
etc.; and (2) exogenous poisons, such as spices, alcohol, ether, chloro- 
form, turpentine, cantharides, salicyl compounds, carbolic acid, minerals, 
mineral acids and salts, etc. In anemic and mild toxemic states degen- 
erative lesions (toxic degeneration of the renal epithelium) are common; 
in severe toxemias and in bacteremias degenerative and inflammatory 
lesions are likely to occur. 

Pathology. — In mild cases, the kidney may be slightly (if at all) 
increased in size, and somewhat opaque (toxic degeneration or cloudy 
swelling); in more severe cases it is perhaps somewhat congested. In 
well-developed acute nephritis it is increased in size, the capsule is 
tense, strips readily, leaving a smooth surface — which in severe cases 
is dark reddish brown in color (hyperemic or hemorrhagic kidney) ; in 
less severe cases and in the subsiding stages of severe cases it is pale 



774 DISEASES OF THE URINARY SYSTEM 

grayish or grayish red in color (anemic kidney); in other cases it ex- 
hibits a combination of these (mottled or variegated kidney). On section 
the organ is usually soft, opaque (as though cooked), cedematous, friable, 
and drips blood; the cortex is swollen and the normal striations obscured; 
the pyramids are usually much congested. The toxins sometimes 
exhibit a selective action, in one case implicating especially the epi- 
thelium of the glomeruli, in another the epithelium of the convoluted 
tubules, in still another the connective tissues. In scarlatina, for instance, 
the glomeruli are likely to be especially involved (glomerulonephritis), 
and may appear as distinct, minute, pale grayish or dark reddish (hemor- 
rhagic) points. Microscopically, the lesions may be confined to the 
parenchyma (toxic degeneration), or they may implicate all the tissues 
(acute diffuse nephritis), or they may be especially conspicuous in the 
interstitial tissue (acute interstitial suppurative or non-suppurative 
nephritis). The parenchymatous lesions consist of cloudy swelling 
(common in most of the acute infections); fatty degeneration (common 
in the severe infections, in certain intoxications such as phosphorus 
poisoning, and in severe anemias) ; hydropsical degeneration and com- 
plete necrosis (which occur in the severest infections, such as cholera, 
and in severe intoxications, such as cantharidal and mercurial poisoning, 
etc.). In addition, in the event of inflammatory lesions, desquamation 
of the renal epithelium commonly occurs (desquamative nephritis), 
and may be excessive. Here and there the lumen of the tubules or of 
Bowman's capsules may be obstructed or distended by swollen and 
desquamated epithelium, coagulated, finely granular albumin, fat 
granules, erythrocytes, leukocytes, tube casts, and detritus. Special 
implication of the tubules or of the glomeruli suggests the terms tubular 
and glomerular nephritis, respectively. The interstitial tissues in the 
merely toxic degenerative cases may reveal no lesions whatever; in the 
more frank or severe cases, dilatation and overfilling of the bloodvessels, 
swelling and oedema of the intertubular connective tissue, and cellular 
exudation and proliferation occur. The lesions, as a rule, are focal 
rather than widespread, and are most marked in the cortex. In some 
cases hemorrhages occur into the tubules, within Bowman's capsules, 
or in the interstitial tissue (hemorrhagic nephritis); in other cases the 
cellular exudation consists largely of polynuclear leukocytes (suppu- 
rative nephritis), and in other cases of Unna's large mononuclear plasma 
cells (acute interstitial non-suppurative nephritis). 

The kidney of pregnancy (to be distinguished from nephritis antece- 
dent to the pregnancy and from an ordinary nephritis, due to the com- 
mon etiological factors developing in a pregnant woman) develops 
especially in young primiparse, in twin pregnancies, and during the latter 
half of pregnancy. Its nature is not well understood, although it is 
probably toxic in origin, the consequence of the maternal kidneys being 
obliged to serve as emunctories for both the mother and the foetus; it 
has been attributed also to perversion of the detoxifying function of the 
liver and of the thyroid, to a toxin elaborated by the syncytium (syncy- 



ACUTE DIFFUSE NEPHRITIS 775 

tiolysins), to bacterial infection and intoxication, to increased intra- 
abdominal pressure exerted especially on the renal veins, the ureters, or 
the cceliac ganglion (occasioning renal anemia in consequence of reflex 
contraction of the renal arteries, etc.). The kidney varies in appear- 
ance in different cases; it may not be distinguishable from the more 
common acute diffuse nephritis; it is enlarged, the capsule strips readily, 
revealing a smooth, pale yellowish or mottled surface. The microscopic 
lesions are largely degenerative, involving the parenchyma; the lesions 
(inflammatory) in the interstitial tissue are comparatively slight. 

Symptoms. — Toxic or degenerative nephritis usually runs its course 
without noteworthy symptoms; the general manifestations of the initi- 
ating infection or intoxication may be not in the least disturbed, and 
the renal condition is recognized only by examining the urine — which 
exhibits the characteristics of so-called febrile urine. It is lessened in 
amount, turbid, of high color and increased specific gravity (1022 to 
1030), and highly acid; it contains an excess of solids and a trace or a 
small amount of albumin (febrile albuminuria), and, depending upon the 
concentration, it deposits more or less sediment that contains a few 
leukocytes and perhaps a few hyaline tube casts. With the subsidence 
of the causative infection or toxic process, the renal conditions and the 
urine usually revert to the normal; in severe cases, however (cholera, 
cantharidal and mercurial poisoning, etc.), anuria may develop and soon 
lead to a fatal issue. 

Acute diffuse nephritis may develop insidiously (as in the infectious 
diseases) or suddenly (as after a debauch and exposure to coldness and 
dampness, severe intoxications, etc.); in either event its existence is 
usually revealed by cedema or changes in the urine, or both; rarely by 
severe uremia (coma, convulsions, etc.). (Edema (due probably to toxic 
alterations of the endothelium of the bloodvessels and capillaries, as 
well as changes in the chloride metabolism, sodium chloride retention) 
is a characteristic sign, and although not invariably present, may be 
detected by careful examination in some cases in which it is thought to be 
absent. It may develop slowly, the patient gradually becoming swollen 
and pale; or it may come on suddenly within twenty-four hours of the 
onset of the disease (especially after a debauch, in scarlatina, etc.). 
It varies much in different cases; it usually develops coincidently with, 
rarely before, the oliguria, but it bears no relationship to the amount 
of urine or of the albuminuria. Usually it develops first in the eyelids, 
then in the face, about the ankles, in the hands, legs, scrotum, and 
loose, areolar, and dependent portions of the body; finally, it may become 
universal (anasarca), involving even the serous sacs (which rarely may 
exhibit collections of fluid before the subcutaneous tissues). (Edema 
of the meninges may occur (and may cause coma, hemiplegia, etc.); 
cedema of the mucous membranes, except perhaps the glottis, palate, 
and conjunctiva, is uncommon; and cedema of the lungs may develop, 
especially in cases proceeding to a fatal issue. 

Diminution in the amount of urine may be the first symptom to attract 



776 DISEASES OF THE URINARY SYSTEM 

attention; the daily amount may be 300 c.c. or less; in some cases com- 
plete anuria supervenes and may lead to a fatal issue. The urine is 
acid in reaction, turbid, highly colored (smoky, rarely bright red, from 
the presence of more or less blood), and of increased specific gravity 
(1024 to 1030); albuminuria (the albumin of the blood serum, serum 
albumin, and globulin; sometimes also nucleo-albumin) is constant — 0.3 
to 1 per cent. (5 to 10 grams) daily; the total output of urea and other 
nitrogenous substances is lessened (although the percentage of urea 
may be increased); the purin bases may be increased. The usually 
abundant (sometimes obviously hemorrhagic) sediment consists of 
erythrocytes (and blood pigment), leukocytes, renal and vesical epi- 
thelium, hyaline, granular, and cellular (epithelial, leukocytic, erythro- 
cytic) casts, compound granule cells, crystals (especially uric acid and 
oxalates), cell detritus, bacteria (not always extraneous contamination), 
etc. The molecular concentration or osmotic pressure of the urine is 
usually reduced (hyposthenuria), so that the freezing point (cryoscopy) 
is 1° or less than 1° C. (instead of the normal 1.3° to 2.3° C.) below that 
of distilled water (0° C). The severity of the urinary changes (amount 
of albuminuria, number and character of the casts, presence or absence 
of blood, etc.) is significant of the severity of the renal changes. 

The general symptoms are not characteristic; local symptoms are 
often in abeyance, although rarely there may be lumbar pain or tender- 
ness, frequent micturition, vesical tenesmus, etc. If the disease develops 
suddenly (as after a debauch) or in children there may be fever (101° 
to 103° F.), associated or not with chilliness, nausea and vomiting, 
headache, and, in children, convulsions; developing during the course 
of one of the infectious diseases there may be (but not necessarily) 
an added increment of fever. Fever, if it occurs, may last for several 
days or a week. The pulse is usually full and of increased tension, 
often slowed in the early, and perhaps accelerated in the later, stages. 
Accentuation of the aortic second sound and some hypertrophy of 
the left ventricle may develop after the lapse of four to six weeks; per- 
haps earlier in children. Epistaxis is a suggestive symptom in some 
cases. Dyspnoea (due to bronchitis, bronchopneumonia, cedema of the 
lungs, hydrothoraXj hydropericardium) may occur, especially in serious 
cases. The appetite is poor, vomiting may ensue (its persistence indi- 
cates the early advent of more ominous uremic symptoms), constipation 
may be present, but diarrhoea is not unusual. Loss of strength and flesh 
are common, but emaciation is usually concealed by cedema. Uremia 
develops and is progressive; the blood is hydremic and of lessened 
specific gravity, and shows the common changes of secondary anemia 
(oligocythemia with lowered color index — disproportionate oligo- 
chromemia); the leukocytes are usually normal, but there may be a 
moderate leukocytosis (16,000 to 22,000), especially in severe cases 
of acute hemorrhagic nephritis, in uremia, and in complicating in- 
fections. The blood becomes toxic, and its freezing point higher than 
normally. Severe uremic manifestations (coma or convulsions) may 



ACUTE DIFFUSE NEPHRITIS 777 

develop at any time, although in acute nephritis, as a rule, they occur 
only when there is marked oliguria. 

Diagnosis. — The diagnosis may be suggested by the history of the case 
and the onset of oedema, but it is made by an examination of the urine. 
Frequent examination of the urine, therefore, should be made in all cases 
in which the likelihood of the development of nephritis is even remote, 
but especially in infections, intoxications, coma, convulsions, and preg- 
nancy. Whether the renal lesions constitute an acute nephritis or (as 
is very common) an acute exacerbation of an already existing subacute 
or chronic nephritis, may be determined in part by the history of the 
patient, and in part by an examination of the urine, especially the sedi- 
ment. 

Prognosis. — The mild degenerative lesions usually subside with the 
initiating infection or intoxication; severe lesions (cholera, yellow 
fever, phosphorus poisoning, corrosive sublimate poisoning, etc.) 
may contribute or lead more directly to a fatal issue (anuria, uremia). 
Acute diffuse nephritis of mild or intermediate grade results in re- 
covery in about 50 per cent, of the cases within four to six weeks; an 
additional percentage of cases pass into the subacute or chronic stage. 
The prognosis is bad in the event of extreme anasarca, marked uremia 
that does not respond promptly to treatment (recovery may ensue), 
and complications (secondary infections, oedema of the lungs, broncho- 
pneumonia, serous membrane transudates and inflammations, etc.). 
The kidney of pregnancy may lead to fatal termination at almost any 
time, but the dangers are much minimized by judicious treatment, 
and recovery usually follows parturition. 

Treatment. — In infections the likelihood of nephritis developing may 
be prevented by the avoidance of exposure to coldness and damp- 
ness; the use of suitable personal and bed-clothing; the non-use of irri- 
tating food and drink; diluting the toxins and other excrementitious 
substances to be eliminated by the kidneys; and promoting the functional 
activities of the skin and intestines. It is said that an imminent attack 
of nephritis manifested by hematuria and increased arterial tension 
may be averted or mitigated by an active cathartic — compound jalap 
powder or a saline cathartic. 

When acute nephritis has developed, we must secure for the patient 
rest, warmth, and a suitable diet; the rest must be absolute and in 
bed until all evidences of the acute manifestations have disappeared. 
He should rest between blankets and wear light flannels — the absence 
of sheets lessens the likelihood of chill and the flannels promote the 
functional activity of the skin. The diet should be for a time at least 
as non-nitrogenous as possible, but of sufficient caloric value. Milk is 
the most suitable, and if possible should constitute. the sole diet for four 
to six weeks; it may be diluted one-third with lime water (which serves 
to decrease the acidity of the urine) or with plain hot water, or an alka- 
line carbonated water, or barley water, or thin oatmeal gruel. The use of 
bland fluids also is serviceable — pure water to which sodium bicarbonate, 



778 DISEASES OF THE URINARY SYSTEM 

potassium citrate, or sodium benzoate (5 to 10 grains, 0.3 to 0.6 gram 
to the ounce) may be added; weak lemonade; a dram of cream of 
tartar, the juice of a lemon, added to a pint of boiling water; thin 
arrowroot, etc. 

Local depletive measures (dry cups, followed by hot linseed poultices 
or other forms of hot moist heat, such as compresses, or the Paquelin 
cautery) sometimes seem to relieve the engorgement of the kidneys; 
they are especially serviceable in cases that begin with local distress, 
hematuria, anuria, etc. 

The use of diaphoretics and purgatives, by promoting the functional 
activities of the skin and the intestines, serve to secure some physio- 
logical rest for the kidneys and to avert the dangers that threaten from 
the accumulation of toxic substances in the blood. Diaphoresis is best 
attained by the use of hydrotherapy — the hot-water bath, the hot-air 
bath, the hot-vapor bath, or the hot wet pack, repeated daily in serious 
cases, but less frequently in less serious cases and as convalescence becomes 
established. The sweating thus induced may be increased by the concur- 
rent administration of a hot drink or a diaphoretic mixture (spirit of 
nitrous ether, solution of ammonium acetate, etc.). In urgent cases pilo- 
carpine also may be used — J to J grain (0.008 to 0.01 gram), repeated 
perhaps in a half-hour if necessary; but it must be employed with 
caution, only when necessary, and it must be avoided in children. Free 
purgation is called for in all cases, and is best attained by the use of 
saline cathartics, compound jalap powder, etc. Calomel should be 
avoided, in the early stage assuredly, since it has a diuretic action 
attained by provoking renal congestion. Similarly, all stimulating 
diuretics are contra-indicated in the early stages. Water is the best 
diuretic; it flushes the kidneys, facilitates the removal of the products 
of inflammation and desquamation, lessens the acidity of the urine, and 
dilutes the toxins in the blood and those passing through the kidneys. 
The bland alkaline diuretics already mentioned may be added to the 
water. In the later stages the more stimulating diuretics, such as 
digitalis, strophanthus, caffeine, cocaine, diuretin, theobromine, etc., 
may be serviceable. 

Special symptoms sometimes demand special treatment. Headache 
may require the use of bromides. Should severe uremic manifestations 
(coma, convulsions) supervene, venesection should be performed, and 
ten to twenty ounces of blood abstracted. In an asthenic subject the 
volume of blood removed may be replaced by an equal volume of physio- 
logical saline solution (half or one-fourth strength in the event of oedema). 
Convulsions not thus relieved may be controlled by a few whiffs of 
chloroform; by chloral (15 to 30 grains, 1 to 2 grams) and potassium 
bromide (60 grains, 4 grams) by the rectum; or by a single hypodermic 
injection (J grain, 0.015 gram) of morphine. In some cases lumbar 
puncture has been efficacious in relieving the convulsions and the coma; 
the cerebrospinal fluid is often under increased pressure in these cases. 
The bowels should be opened immediately and freely, by an enema and 



ACUTE SUPPURATIVE NEPHRITIS 779 

by the use of croton oil (2 drops) in olive oil on the back of the tongue, 
or elaterium (J grain, 0.015 gram). Profuse sweating also should be 
induced by a hot wet pack or a hot-vapor bath. Vomiting and diar- 
rhoea (uremic phenomena) often subserve a useful purpose of elimination, 
and should not always be immediately checked. Vomiting, if exhausting, 
should be met with counterirritation to the epigastrium, and bismuth, 
cerium oxalate, creosote, carbolic acid, dilute hydrocyanic acid, sips 
of very hot water, cracked ice, etc. Anasarca that does not yield to 
measures already mentioned may require small incisions into the skin 
or the use of Southey's tube; often, however, it can be markedly, if not 
altogether relieved by the use of a salt-free (or salt-poor) diet (bread, 
meat, potatoes, eggs, etc., cooked and eaten without salt). Transudates 
in the serous cavities should be tapped. Pulmonary oedema, broncho- 
pneumonia, and other complications are to be treated on general prin- 
ciples. During convalescence care should be taken to avoid chill and 
possible relapse (avoidance of exposure; use of flannels, etc.). The 
diet should be gradually augmented; first, farinaceous foods, then light 
vegetables, non-acid fruits, meats, etc. Anemia and weakness suggest 
the use of iron (liquor ferri et ammonii acetatis) and strychnine, but 
iron should not be employed unless there is anemia, nor until the acute 
manifestations have subsided. 



ACUTE SUPPURATIVE NEPHRITIS. 

(Acute Hematogenous Infection of the Kidney.) 

Etiology. — Infection of the kidney leading to suppuration may be pro- 
voked by staphylococci, streptococci, pneumococci, gonococci, colon 
bacilli, typhoid bacilli, tubercle bacilli, etc. Infection may occur (1) by 
way of the blood stream; (2) by way of the ureter— pyelonephritis 
(page 788); or (3) by contiguity or continuity of tissue — perinephritic 
abscess (page 792). The hematogenous infections constitute a special 
form of nephritis. The condition may be apparently primary, and 
of traumatic or undiscoverable cause; or it may be secondary, and 
follow one of the infectious diseases (typhoid fever, diphtheria, etc.); 
septicopyemia or a single suppurative focus (furuncle, phlegmon, 
osteomyelitis, erysipelas, etc.); or some intestinal infection, especially 
in children. 

Pathology. — The lesions consist of foci of suppuration in varying 
stages of development — from mere leukocytic accumulations to well- 
marked necroses and small, usually miliary abscesses; these are usually 
situated in the cortex, and although they are usually bilateral, they are 
often unilateral. 

Symptoms. — The symptoms consist of the antecedent disorder (in- 
fectious disease, localized suppuration, etc.), to which, at the time of 
infection of the kidney, sudden increase of fever, chills or chilliness, 
perhaps sweating, and leukocytosis are added; and to these also local- 



780 DISEASES OF THE URINARY SYSTEM 

izing signs, such as abdominal pain, tenderness over one or both kidneys 
anteriorly, and tenderness and muscular rigidity at one or both costo- 
vertebral angles posteriorly (especially significant if unilateral). The 
urine, as a rule, is somewhat reduced in amount, and contains albumin, 
pus, blood, and casts. In some severe hyperacute cases the onset is 
sudden and severe, prostration is marked, fever is high (104° to 106°), 
and the general picture corresponds with that of general septicopyemia 
and obscures the local phenomena referable to the kidney. In less severe 
or subacute cases there are more or less protracted chills, fever, sweats, 
leukocytosis, and unilateral costovertebral tenderness and muscular 
rigidity. 

Diagnosis. — The diagnosis is often uncertain, but may often be made 
by attention to the etiological factors, the local signs, the urinary 
changes, and the absence of any vesical or renal pelvic condition that 
might cause urogenous infection of the kidney tissue (cystopyelitis and 
pyelonephritis). 

Prognosis. — The prognosis depends upon the etiological factors and 
whether the condition is unilateral or bilateral. 

Treatment. — The treatment, in general, is that of septicopyemia. 
The local lesions may be favorably influenced by bacterins corresponding 
to the infection. In unilateral infections not otherwise remediable, 
resort should be had to surgical intervention. 



CHRONIC DIFFUSE NON-INDURATIVE NEPHRITIS. 

(Subacute and Chronic Parenchymatous Nephritis; Chronic Bright' s Disease.) 

Etiology. — Chronic diffuse non-indurative (or parenchymatous) nephritis 
is most common in young male adults between the ages of twenty and 
forty years; but it is not rare in women, and in children especially after 
scarlatina. It may follow acute nephritis, and has then a like etiology 
and pathogenesis. Perhaps in most cases it develops insidiously, sub- 
acutely, or chronically, and is attributed to continued or repeated expo- 
sure to the inclemencies of the weather, insanitary surroundings, over- 
indulgence in alcohol, or infective or toxic agents insufficient in amount 
or virulence to cause acute nephritis (malaria, tuberculosis, syphilis, 
prolonged suppuration, in which event it may be associated with amyl- 
oidosis, etc.). Although the course is chronic, acute exacerbations are 
common; indeed, many cases of so-called acute nephritis are likely 
acute exacerbations of previously unrecognized subacute or chronic 
nephritis. 

Pathology. — The lesions are not essentially different from those of 
acute nephritis, except in the addition of secondary alterations, the 
development of which requires time. Two types of kidneys occur — the 
large white (more properly pale or yellow) kidney, and the large red, 
mottled, or variegated kidney. Both are enlarged (the yellow more 
so than the red) ; the capsule strips readily, revealing a smooth surface — 



CHRONIC DIFFUSE NON-INDURATIVE NEPHRITIS 781 

pale yellowish, or mottled grayish yellow, or reddish yellow, in the one; 
and grayish red or mottled (commonly of pale and dark areas) or very 
dark reddish brown or hemorrhagic, in the other (chronic hemorrhagic 
nephritis). The cortex is swollen and pale, mottled, or dark red, and 
hemorrhagic. Should the patient survive eighteen months or more, 
the lesions of indurative nephritis gradually develop (secondarily con- 
tracted kidney). Microscopically, the glomeruli exhibit proliferative and 
degenerative changes, involving the epithelium and the endothelium, 
similar to those of acute nephritis; the changes in the tubular epithelium 
are especially marked in the convoluted tubules, and are similar to 
those of acute nephritis, fatty degeneration, however, being conspicuous 
(fatty degeneration and anemia being largely responsible for the pallor 
of the kidney). The changes in the interstitial tissue are similar to those 
of acute nephritis, usually, however, less active, more advanced; in some 
cases there is considerable hemorrhage (acute exacerbations; chronic 
hemorrhagic nephritis). In the course of time the cellular exudate 
becomes converted into newly formed fibrous connective tissue, which by 
contracting leads to atrophy of the glomeruli and tubules (secondarily 
contracted kidney). 

Symptoms. — The disease may develop out of acute nephritis — pallor, 
dropsy, and albuminuria persisting. Usually it develops insidiously. 
The patient may complain of gradual failure of health, loss of flesh and 
strength, headache, pallor, indigestion, with periodic attacks of nausea 
and vomiting, etc.; or swelling of the eyelids, feet, or ankles; or cloudiness 
and lessened amount of urine may attract his attention; or albuminuria 
may be detected accidentally (examination for life insurance, etc.). 
As in acute nephritis, the characteristic signs consist of oedema (which 
rarely may be absent) and of changes in the urine. At first the oedema 
is usually slight, but it varies much in different cases; it partakes of the 
characteristics already mentioned in connection with acute nephritis, 
and having disappeared is likely to recur. The urine is lessened in 
amount (usually 300 to 700 c.c), acid in reaction, turbid, of varying 
color (depending upon the concentration and the amount of contained 
blood), of increased specific gravity (1018 to 1025), contains considerable 
albumin (1 to 3 per cent.; i to f by bulk after the heat and acid test; 
15 to 30 grams in the twenty-four hours); the excretion of solids is 
deficient; the sediment is usually abundant, and consists of: erythrocytes 
and leukocytes; epithelium from the uriniferous tubules, the renal 
pelvis, and the bladder; hyaline, granular, and cellular (epithelial, 
fatty, leukocytic, and sometimes erythrocytic) casts; waxy casts (in 
associated amyloid disease); compound granular cells, fat droplets, 
detritus, bacteria, etc. The general symptoms are much like those 
mentioned in connection with acute nephritis. Debility and anemia 
are usually marked, the anemia seemingly bearing some relationship 
to the rapidity of the renal lesions. Chronic uremic (especially nervous 
and gastro-intestinal) symptoms are common and persistent, although 
subject to remissions and exacerbations; acute uremia is less common 



782 DISEASES OF THE URINARY SYSTEM 

than in acute nephritis and chronic indurative nephritis. The blood 
pressure is usually increased, and hypertrophy of the heart and 
arteriosclerosis often supervene. Albuminuric neuroretinitis is quite 
common. 

Diagnosis. — The diagnosis is suggested by the history of the case, 
pallor, and oedema, but it must be based upon an examination of the 
urine. Much fat (fatty casts, free fat droplets, etc.) suggests the pale 
kidney; blood, the red or mottled kidney — an acute exacerbation. 
The amyloid kidney is suggested by the etiological factors of amyloid 
disease, enlargement of the liver and spleen, relatively slight oedema, 
relatively few casts (and these hyaline, waxy, and granular), little or 
no hypertrophy of the heart, and the absence of uremia and of neuro- 
retinitis. The advent of secondary renal contraction leads to symp- 
toms that will be mentioned under chronic indurative nephritis. 

Prognosis. — The duration of the disorder commonly varies from 
several months to two years or thereabouts; remissions and exacer- 
bations are common; some patients gradually developing a secondarily 
contracted kidney may survive for a number of years. The outlook 
however, is always gloomy, since recovery is extremely rare. The prog- 
nosis is the worse the greater the degree and persistence of albuminuria, 
oedema, and uremic manifestations, the less the excretion of urinary solids, 
and the more marked the cardiovascular changes, the neuroretinitis, and 
other complications. 

Treatment. — The treatment, hygienic, dietetic, and medicinal, is 
similar to that of acute nephritis. From time to time a strict milk diet 
is valuable. In other cases with marked oedema benefit accrues from 
a salt-poor diet; at all events, as little salt as possible should be given. 
The oedema may also be favorably influenced and perhaps the ten- 
dency to uremic manifestations lessened in some cases by Basham's 
mixture; or by Trousseau's diuretic wine: 

1$ — Powdered digitalis '. .... 1 dram 4 

Powdered squill \ dram 2 

Juniper berries 5 drams 20 

Potassium acetate 2 drams 8 

White wine 6 ounces 200 0— M. 

S. — One tablespoonful (15 c.c.) 3 or 4 times daily. 

or by Grainger Stewart's mixture: 

1$, — Potassium acetate 2 drams 8 

Infusion of digitalis 3 ounces 100 JO 

Infusion of scoparius 3 ounces 100,0 — M. 

S. — One tablespoonful (15 c.c.) 3 or 4 times a day. 

Strontium lactate, diuretin, theobromine, sparteine, etc., may render 
service from time to time. Renal decapsulation has been practised with 
good results in some cases. The treatment of uraemia is mentioned on 
page 778. 



CHRONIC DIFFUSE INDURATIVE NEPHRITIS 783 



CHRONIC DIFFUSE INDURATIVE NEPHRITIS. 

(Chronic Interstitial Nephritis; Arteriosclerotic Kidney; Chronic Bright' s Disease;) 
Cardiovascular-renal Disease.) 

Etiology. — Chronic diffuse indurative (or interstitial) nephritis may be 
primary or secondary. The primary condition occurs especially after 
the fortieth year, but it may occur even in children. It is twice as com- 
mon in men as in women. The disease is largely the result of the 
exigencies of modern life : the hurry and the cares, the worries and the 
anxieties of modern life, the nervous tension and the mental strain in- 
separable from large undertakings, heavy financial responsibilities, and 
high society. An irregular mode of life, overeating of rich and highly 
seasoned food, excessive indulgence in alcohol, and insufficient muscular 
exercise tend to increase blood pressure and to pervert metabolism, the 
products of which being eliminated by, irritate and cause progressive 
deterioration of, the chief emunctories, the kidneys. In some cases the 
disease is directly attributable to certain autogenous and exogenous 
poisons, such as alcohol, gout (gouty kidney), lead, etc.; and sometimes 
the disease seems more or less related etiologically to certain infections, 
such as syphilis, malaria, etc. The causes of the disease in general are 
those of arteriosclerosis, which is apparent in the separation of a special 
type of the disease (arteriosclerotic kidney) believed to originate in the 
bloodvessels rather than in the kidneys; in another class of cases the 
lesions appear to be merely those of advancing age (senile kidney). 
The phenomena in most cases are correctly interpreted by recognizing 
that the disease is not a disease of the kidneys alone, perhaps not even 
primarily, but a disease of the cardiovascular system and the kidneys 
(cardiovascular-renal disease). Secondary chronic diffuse indurative 
nephritis develops, as a rule, secondarily to the large white kidney; its 
etiology, therefore, is that of the antecedent condition. 

Pathology. — In the primary (and the arteriosclerotic) process the 
kidney is much reduced in size (both together may weigh less than 
50 grams); the capsule is thickened and markedly adherent, and when 
removed reveals a dark reddish brown, markedly granular surface, 
containing, as a rule, a variable number of small cysts; the organ is firm 
hard, and dense; the cortex is much reduced in thickness (to 2 mm.). 
The arteries show more or less sclerosis. Microscopically, the con- 
spicuous change is an overgrowth of cicatricial fibrous connective 
tissue with associated (consecutive) atrophic and degenerative changes 
in the parenchyma. The fibrosis is especially marked about Bow- 
man's capsule and the small arteries — whence it spreads to the adjoining 
tissues; the Malpighian bodies ultimately may be represented by 
a functionless, roundish, hyaline mass, and the small arteries may 
become completely fibrosed and their lumens occluded. Obstruction 
and occlusion of uriniferous tubules give rise to the formation of 
small cysts. In the arteriosclerotic kidney the lesions are believed to 



784 DISEASES OF THE URINARY SYSTEM 

originate in the bloodvessels, but it is often quite impossible to dis- 
tinguish between the two forms of the disease — if there really be two 
forms. The secondarily contracted kidney is sometimes slightly en- 
larged, sometimes normal, and sometimes somewhat reduced in size; 
it is firm and hard; its capsule is thickened and adherent, and when 
removed reveals a granular pale yellowish or mottled yellowish-red 
surface, containing a variable number of small cysts; the cortex is 
thinned. Microscopically, to the lesions of the large white kidney are 
added overgrowth and cicatrization of connective tissue, more or less 
fibrosis and obliteration of the glomeruli, arteriosclerosis and obliter- 
ating endarteritis, occluded and distended uriniferous tubules (cysts), 
etc. In addition, in all forms of chronic indurative nephritis there 
is more or less widespread arteriosclerosis, and hypertrophy, and later, 
dilatation of the heart (page 437) ; and perhaps fibrosis elsewhere in the 
body. 

Symptoms. — The symptoms of primary chronic indurative nephritis 
develop as insidiously as do the lesions in the kidneys and the cardio- 
vascular system. The disease may exist for years entirely devoid of 
symptoms; it may be detected accidentally in a routine examination 
of the urine for life insurance or other reason; or it may give rise to an 
extremely variable set of initial symptoms that are likely to be attrib- 
uted to some organ other than the kidneys. Thus, the patient may 
present himself to his physician with the idea that he is suffering with 
diabetes on account of the large amount of urine that he voids; or he 
may complain of dimness of vision, the consequence of albuminuric 
neuroretinitis; or of one of the many manifestations of chronic uremia, 
such as dyspnoea or asthma; or of gastro-intestinal derangements, 
such as gastric catarrh, gastric hemorrhage, or diarrhoea; or of headache, 
hemicrania, tinnitus aurium, vertigo, neurasthenia, pains in the muscles 
or joints, or eczema; or palpitation of the heart and precordial distress; 
or, the patient in apparently good health, may suddenly develop a severe 
and even fatal attack of cardiac failure, or he may pass into uremic 
coma or convulsions, or he may suffer an apoplexy and die. 

Variable as are the modes of onset, the diagnosis of the disease depends 
upon an examination of the urine and of the cardiovascular system. The 
urine is increased in amount — 1800 to 4000 c.c. daily — whence the common 
complaint of frequent micturition and sometimes of increased thirst; 
it is acid in reaction, pale in color, and of low specific gravity (1002 to 
1015); it contains a slight amount of albumin — usually only a trace, 
and at times no albumin at all. Albumin may be absent for days and 
even weeks at a time; it may be missed in the early morning urine and 
be present in that voided later in the day; and it may be present only 
after exercise, emotional and other excitement, or after eating, especially 
after eating proteins. The urine deposits a slight flocculent sediment 
that contains a few, sometimes a very few (often very narrow), hyaline 
and pale granular casts, and a few epithelial cells, mostly from the 
bladder. The solids of the urine are usually diminished. 



CHRONIC DIFFUSE INDURATIVE NEPHRITIS 785 

The characteristic cardiovascular signs consist of increased blood 
pressure (an early and valuable sign), arteriosclerosis, accentuation 
of the aortic second sound, and hypertrophy of the heart, especially 
the left ventricle (sometimes obscured by co-existing emphysema). 
Although these cardiovascular signs may be found in all forms of Bright's 
disease (but not in all cases), in none of the forms do they so dominate 
the clinical picture as in primary chronic interstitial nephritis. So long 
as the nutrition of the heart is well maintained there may be no symp- 
toms, although for months or years dyspnoea and palpitation of the heart 
may be provoked by exertion or excitement. As the nutrition of the 
heart begins to lag behind its enlargement, degeneration and dilatation 
ensue and symptoms of embarrassed circulation become ascendent — 
cardiac asthma, congestion and oedema of the lungs, bronchitis, gastro- 
intestinal disturbances, generalized oedema and effusions within the 
serous cavities, and alterations in the urine: it lessens considerably in 
amount and becomes of high color and increased specific gravity; 
albumin increases in amount and casts become more numerous; dark 
granular, epithelial, and even blood casts and free erythrocytes may be 
encountered. The symptoms referable to the heart and lungs, at first 
transitory and nocturnal, become permanent; the blood pressure lessens; 
the aortic second sound becomes less accentuated; with embarrassment 
of the right heart the pulmonary second sound becomes at first accent- 
uated, and later fails ; signs of dilatation, and gallop rhythm, always of 
serious moment, supervene; and if relief is not afforded, death ensues 
with cardiac failure or uremia, or both, dominating the final scene. 

In some cases the first suggestive symptom may be oedema of the lungs 
or of the larynx; the dyspnoea due to one or both of these may be 
augmented by hydrothorax; Cheyne-Stokes breathing may ensue, and 
in coma the patient may die. Or the first symptom may be violent head- 
ache — due either to uremia, cerebral congestion, or cerebral anemia. 
The headaches are occasionally relieved by epistaxis, which is some- 
times frequent and sometimes severe. Drowsiness and other nervous 
manifestations of chronic uremia may be associated with the headache, 
and frequently presage the onset of severe, acute, and fatal uremia. 
In some cases psychoses are prominent; in other cases neuralgias or 
hemorrhages into the brain substance or into the meninges may occur. 
Hemorrhages into other structures, especially the stomach, intestine, 
skin, conjunctiva?, lungs, etc., have been observed. Severe and un- 
controllable vomiting and severe and exhausting diarrhoea are not 
uncommon. In other cases the disease is manifest by intolerable itching, 
formication, numbness of the extremities; in still other cases, by urticaria. 
In the late stages more or less widespread erythematous, or bullous, or 
desquamative skin lesions may occur. Neuroretinitis is the most 
important symptom on the part of the special senses; at times tinnitus 
aurium, possibly associated with dizziness, occurs; less frequently deaf- 
ness or diplopia ensues. 

Secondary chronic interstitial nephritis (the small white kidney) 
50 



786 DISEASES OF THE URINARY SYSTEM 

is usually only with difficulty differentiated from its antecedent stage 
(the large white kidney). Presumptive evidence of secondary contrac- 
tion of the kidney, however, is afforded by long duration of the disease 
(more than a year), lessening of dropsy, lessening of albuminuria, 
increase in the daily excretion of the urine, and decrease in the specific 
gravity, and the development and progression of the cardiovascular 
signs of chronic interstitial nephritis. 

Diagnosis. — As long as cardiac compensation is maintained, the 
diagnosis of chronic indurative nephritis is evident from the results of 
an inquiry into the antecedents of the patient, the special etiological 
factors in the case, the course of the disease, the different clinical manifes- 
tations, and an examination of the urine and of the cardiovascular 
apparatus. The diagnostic importance of the cardiovascular alterations 
cannot be overestimated. They are among the earliest clinical 
manifestations of the disease, and they may be detected even in the 
absence of positive signs of kidney disease on the part of the urine. 

It is usually a matter of extreme difficulty to distinguish clinically 
between primary chronic interstitial nephritis and the arteriosclerotic 
kidney; in some cases it is impossible, in most cases it is unnecessary. 
Usually the arteriosclerotic kidney exists for a long time without albu- 
minuria, or with but the slightest trace of albumin in the urine. The 
disease may be suspected in elderly persons, with hypertrophy of the 
heart, increased arterial tension, and marked atheroma of the superficial 
arteries. Occurring as a manifestation of senility, it is usually of relative 
unimportance as contrasted with the co-existing emphysema, dementia, 
marasmus, etc. 

When the heart begins to fail in chronic interstitial nephritis, diag- 
nostic difficulties arise. The clinical picture in these cases much re- 
sembles that of a disorder primarily cardiac and secondarily renal. The 
presence of murmurs is not conclusive evidence, since they may be due 
to dilatation as well as to valvular disease. Diastolic murmurs, however, 
suggest a primary cardiac disorder, whereas albuminuric neuroretinitis 
suggests a primary renal disorder. In some cases the diagnosis, for a time 
at least, is impossible; in other cases it may be made by a careful analysis 
and balancing of all the features of the case, by a knowledge of the past 
history of the patient, and by the results of administering digitalis and 
other heart tonics. Following the administration of digitalis, should the 
patient improve materially, the urine increase in amount, and albumin 
and casts finally disappear from the urine, the condition has been defi- 
nitely determined to have been primarily cardiac with secondary renal 
congestion. If, however, with improvement in the condition of the heart, 
albumin and casts do not disappear from the urine, one may be confident 
of the existence of nephritis, a conviction that may be confirmed by 
examining the cardiovascular apparatus now that compensation has 
been restored. It is scarcely likely that chronic indurative nephritis 
will be confounded with the so-called functional, physiological, cyclic, 
intermittent, paroxysmal, or adolescent albuminuria. 



CHRONIC DIFFUSE INDURATIVE NEPHRITIS 787 

Prognosis. — In. general the prognosis depends upon the integrity of 
the cardiovascular apparatus. The disease may run a course entirely 
latent and lead to sudden death by apoplexy, acute uremia, etc. Ordi- 
narily, however, the course is from ten to twenty years, depending upon 
the habits and mode of life. When the circulation becomes embarrassed 
the prognosis is bad; lessening in the amount of urine, especially if 
associated with headache, often presages the speedy onset of acute uremia. 

Treatment— In the early stages of the disease, appreciating our in- 
ability to cure our patient, we should be alert to the dangers that threaten 
him (rupture of small arteries, especially of the brain, uremia, cardiac 
failure). He must be cautioned not to expose himself to the inclemencies 
of the weather, to avoid all excessive muscular exercise and all mental 
worry; he must have his bowels open at least once daily (alkaline mineral 
waters, saline cathartics, occasional blue mass pill, etc.); and he must 
favor the action of the skin so as to relieve the subnormal cardiovascular- 
renal system; warm or hot baths are serviceable, but they are contra- 
indicated if they cause unpleasant throbbings (increasing blood pressure). 
The diet is of the utmost importance, the duration of life probably 
depending more upon discretion in eating and drinking than upon any 
other factor. In many cases an exclusive milk diet for a time (four to 
six weeks) is desirable; and it may be repeated from time to time. In 
general the diet should be sufficiently varied to be attractive, it should 
be free from irritating qualities and readily assimilable, and the nitrog- 
enous constituents should be relatively reduced. The meat allowance 
should not exceed 100 grams daily; a diet of ample fuel value should be 
constructed by adding a sufficiency of fats and carbohydrates; an excess of 
meat is said to favor the development of uremia; red and white meats 
are of equal value, and may be allowed in accordance with the patient's 
desires. As a rule, alcohol should be prohibited, although in some cases 
a little of the lighter wines appears to do no harm. In many cases the 
foregoing produces not only amelioration of the symptoms, but perhaps 
also arrest of the lesions; if so, other measures are not required. 

When the circulation becomes embarrassed medication is called for — 
the most serviceable remedies being nitroglycerin and caffeine. Nitro- 
glycerin lowers the arterial tension and enables the heart still capable 
of performing its work to do so unhampered by excessive resistance in 
the arterial tree; it is said also to favor reduction in the amount of albu- 
min excreted, but this action is doubtful and certainly immaterial. 
This dose may be increased until the desired result is obtained. It is 
not necessary that the drug be given to the extent of producing unpleas- 
ant symptoms; sufficient reduction in the arterial tension is usually 
produced without this. Nor is great reduction in the arterial tension 
desirable; indeed, it is directly contra-indicated, since a reduction 
even to that of the normal tension is fraught with danger of serous 
effusions, and of uremia (on account of reduction in the amount of 
urine excreted). The nitroglycerin should be given for four to 
six weeks and then discontinued for a week or ten days, unless the 



788 DISEASES OF THE URINARY SYSTEM 

condition of the patient should render an earlier return to its use neces- 
sary. The nitrite of potassium or of sodium or erythrol tetranitrate 
may be substituted for the nitroglycerin, but they are less efficacious. 
Inasmuch as the nitrites interfere somewhat with the oxygenating powers 
of the blood, their continuous administration should not be persisted in too 
long. Iodide of potassium or of sodium in small doses, mercuric bichlor- 
ide, and chloride of gold and sodium are still advocated; in some cases 
good results appear to attend their prolonged use. It is difficult, how- 
ever, to estimate the amount of good that with justice may be attributed 
to their use. In the absence of serious cardiac debility, cardiac stimu- 
lants, such as digitalis and strophanthus, should not be given. Nor 
is the routine administration of iron to be countenanced. Anemia is 
rarely marked, and any virtues that iron may possess are outweighed 
by certain ill effects, such as its tendency to constipate, to produce head- 
aches, etc. However, should anemia become marked, iron may be given 
in small doses. Quinine, strychnine, and arsenic are often of service 
in this stage of the disease, as well as earlier. Renal decapsulation is 
sometimes of service. 

When marked cardiac debility and manifest failure of compensation 
develop (generalized oedema, effusions in the several serous cavities, dimi- 
nution in the amount of urine, increase in the amount of albumin, etc.), 
digitalis and other cardiac stimulants should be given. In general, 
the treatment of this stage of the disease does not differ from that already 
recommended in connection with acute and chronic non-indurative 
nephritis, and from that commonly practised in cases of lack of cardiac 
compensation. Impending uremia, manifest by headache, restlessness, 
foul breath, coated tongue, vertigo, etc., may be warded off by nitro- 
glycerin and caffeine, saline cathartics, alkaline diuretics, large amounts 
of water, hydrotherapeutic measures, and restriction of the diet to milk. 
In some cases digitalis is urgently called for. The treatment of acute 
uremia developing in the course of chronic indurative nephritis does 
not differ from that already mentioned (page 778). 



CYSTITIS; URETERITIS; PYELITIS; PYELONEPHRITIS; PYELO- 

NEPHROSIS. 

Etiology. — Inflammation of the bladder, the ureter, and the renal 
pelvis may occur singly or in combination ; the inflammatory phenomena 
may ascend from a part of the urinary tract low down to that high up, 
or they may descend; and they may be acute or chronic. Although many 
bacteria have been described in these urinary infections, the most 
important are the typhoid and colon bacilli (acute and chronic infec- 
tions), gonococci, staphylococci, streptococci, and pneumococci (acute 
infections), the tubercle bacillus (chronic infections), and perhaps also 
certain anaerobic organisms. Ascending (urogenous) infections of 
the bladder are usually preceded by urethritis (or vaginitis), commonly 



CYSTITIS 789 

gonococcic; they may result from the introduction into the bladder of 
infected foreign bodies (catheters, etc.); or they may be due to the transit 
of infectious agents (commonly the colon bacilli or the pyococci) from 
the rectum or other pelvic viscus directly to the bladder (transparietal 
route). Thence the ureters, the renal pelves, and the kidneys themselves 
may become infected, commonly by progressive ascending infection of 
the mucosa; rarely by the transit of the infectious agent through the 
blood stream or the lymph stream. Descending infections— the con- 
sequence of the elimination of bacteria by the kidneys (therefore hema- 
togenous infections) — occur under circumstances similar to those that 
induce suppurative nephritis (page 779); they are usually due to the 
typhoid bacillus, the colon bacillus, proteus vulgaris, the pyococci, etc. 
Pyelitis may be the initial lesion, but in some cases the bacteria pass 
through, apparently without injuring, the pelvis, and may first set up a 
cystitis. As is well known, the mucosa of the urinary tract is remarkably 
resistant to the influence of bacteria eliminated with the urine. Appar- 
ently healthy kidneys may excrete bacteria (as in many infections, 
notably typhoid fever), and these may be discharged from the body, 
without damage to the urinary tract. Certain predisposing factors 
seem operative in many cases, and may determine the primary local 
infection — such as trauma, arteriosclerosis, diabetes, a calculus (in the 
renal pelvis or the bladder), enlarged prostate, urethral stricture, 
ammoniacal decomposition of the urine, a pelvic tumor, a pregnant 
uterus, the excretion of irritating drugs, etc. 

Pathology. — The lesions may be catarrhal, suppurative, or ulcerative; 
unilateral or bilateral; and acute or chronic. In the catarrhal process 
there is swelling, oedema, and congestion of the mucosa, with the exces- 
sive formation of mucus; in aggravated cases considerable mucopus 
or almost pure pus is formed, and there is more or less desquamation 
and superficial erosion of the epithelium and foci of hemorrhage; or 
more or less widespread and deep ulceration may occur. In the chronic 
cases there is, in addition, more or less thickening and pigmentation. 
Rarely fibrinous exudations or gangrene ensue. There is, as a rule, more 
or less decomposition of the urine with the precipitation of urates and 
phosphates. When the infection extends from the renal pelvis to the 
kidney substance (urogenous pyelonephritis) yellowish purulent streaks 
are found extending from the papillae into the medulla and the cortex, 
and small miliary abscess throughout the kidney, but most numerous 
in the cortex just beneath the surface and arranged often in groups. 
In the event of obstruction in the renal pelvis, the ureter, bladder, 
or urethra, with consequent increased intrapelvic (renal) pressure, the 
pelvis and calices become distended, the renal tissue more or less de- 
stroyed, and the kidney ultimately converted into an intercommuni- 
cating, many-chambered pus sac (pyonephrosis) lined by the remains 
of the pelvic mucosa; should this become very large, very little kidney 
tissue may be demonstrable (degeneration, atrophy, and replacement 
by connective tissue). 



790 DISEASES OF THE URINARY SYSTEM 

Symptoms. — The symptoms vary with the site and progression of the 
lesions; in some cases, especially in children, there may be no symptoms 
whatever referable to the urinary tract. 

Acute cystitis, as a rule, is manifested by pain in the region of the 
bladder developing spontaneously, augmented by urination, and radiat- 
ing to the urethra; strangury and vesical tenesmus; and local tender- 
ness. Occasionally, in consequence of sphincter spasm or urethral 
obstruction by a plug of mucus, there may be retention (ischuria). 
The general phenomena consist of fever, perhaps chill or chilliness 
(at the beginning of acute cases), leukocytosis, headache, malaise, 
etc. In subacute and chronic cystitis the local and general phenomena 
are less marked and may be quite in abeyance. The urine when voided 
may be acid or alkaline depending upon the infecting organism : acid in 
colon-bacillus infections, and alkaline in infections by urea-decomposing 
organisms. Furthermore, the urine contains more or less mucus, pus, 
erythrocytes, albumin (proportionate to the pus and blood), bladder 
epithelium, perhaps particles of necrotic bladder mucosa, many bacteria, 
and in the event of alkaline decomposition (urea-decomposing organisms), 
triple phosphates, ammonium urate, etc. Cystoscopic inspection of 
the bladder reveals the inflammatory lesions; in the chronic process — 
often tuberculous ulcers. The thickening that develops in chronic 
cases may be palpable — above the pubes; or bimanually — vaginal 
(or rectal) and suprapubic. Acute cystitis lasts for several days to several 
weeks, and may then subside entirely, or go on to the chronic stage; 
this may continue for months or years, and ultimately lead to ascending 
infection of the urinary tract. 

Ureteritis is rarely if ever an independent affection; usually it is part 
of, or associated with, cystitis and pyelitis. Local pain, tenderness, 
and palpable thickness along the course of the ureter can sometimes be 
made out, and cystoscopic examination of the bladder often reveals 
excessive inflammatory phenomena at the mouths of, and perhaps 
some distance into, the ureters. 

Pyelitis and pyelonephritis are manifested, as a rule, by impairment 
of the general health, by more or less obtrusive symptoms of septi- 
copyemia, and by certain local signs. In the milder cases (subacute 
or chronic urogenous pyelitis or pyelonephritis) fever may be mild 
(99° to 100°) but more or less continuous; there may be a tendency to 
ready sweating; slight leukocytosis is likely to be present; anemia de- 
velops and progresses. In some cases, suddenly chills, fever, and sweats 
supervene and the leukocytosis increases; the fever may reach a high 
grade (104° or more), continue for several days or a week or more, and 
gradually subside to the previous grade. At varying intervals, such an 
attack may recur (recurring type). In addition there may be local pain 
(often spontaneous and colicky) and tenderness in the region of the kid- 
ney (or kidneys), frequent micturition, and in the event of pyelonephrosis 
a variable-sized, tender, fluctuating mass in the region of the kidney. 



CYSTITIS 791 

The urine contains mucus, pus, erythrocytes, albumin (proportionate 
to the pus and blood), fibrinous plugs, caudate epithelium from the 
renal pelvis (not always recognizable) and other epithelium, and crystals, 
often corresponding to a calculus in the renal pelvis, but otherwise 
varying with the alkalinity or acidity of the urine. The amount of urine 
varies much in some cases, being often reduced and then suddenly 
increased — associated with release of an obstruction and discharge 
of accumulated urine, lessening in size of the palpable fluctuating 
tumor, and subsidence of the general manifestations of toxemia. In 
chronic cases there may be presistent polyuria (usually due to secondary 
chronic interstitial nephritis). 

Diagnosis. — The diagnosis of infection of the urinary tract is easy 
in the great majority of cases; but some difficulty may be experienced 
in determining the seat and extent. Cystitis is readily recognized by 
vesical pain and tenesmus, strangury, and the condition of the urine; 
and outspoken pyelitis by pyuria (especially intermittent pyuria), pain, 
tenderness, and a fluctuating mass in the region of the kidney. In many 
cases, however, these are not obtrusive, and the diagnosis depends 
upon the differential interpretation of pyuria; this is especially the case 
in marked toxemias or infections which are common in children, during 
pregnancy and the puerperium, etc. — whence the importance of examin- 
ing the urine in all obscure febrile conditions, particularly those without 
any localizing symptoms. In some cases, special importance attaches 
to an antecedent enlarged prostate, urethral stricture, etc. Pressure 
on the kidney and massage in the direction of the ureter may lead to the 
discharge of pus into the bladder — which may be observed by means 
of a cystoscope. Effort should always be made to determine the nature 
of the infection; the tubercle bacilli may be recovered in many cases 
not thought to be tuberculous. More albuminuria than can be explained 
by the pus and blood suggests concurrent nephritis. 

Prognosis. — The prognosis depends upon the nature of the infection — 
tuberculous or non-tuberculous, and whether simple or associated with 
a calculus. In acute cases the prognosis, as a rule, is good; chronic 
cases may last for years. 

Treatment. — Efforts should be made to prevent the infection — by 
the use of clean catheters, etc. ; by prompt and efficient treatment of 
gonorrhoea, vaginitis, cystitis, etc; and when the urinary tract is damaged, 
by avoiding irritating drugs that must be eliminated by the kidney; 
etc. The developed infection should be met by bland fluids (milk, water, 
mineral waters) to flush the urinary tract, and urinary antiseptics, such 
as hexamethylenamin, salol, sandal oil, etc. In urinary acidity (colon 
bacillus infections), potassium acetate and citrate and sodium benzoate 
are of much service. Autogenous vaccines corresponding to the infecting 
organism are of much value in many, especially, protracted cases. 
Local warm applications afford relief in cystitis. In protracted cystitis 
irrigations with mild antiseptics should be used; or persisting ulcerations 



792 DISEASES OF THE URINARY SYSTEM 

(usually tuberculous) may require the local application (through the 
cystoscope) of lactic acid, etc. Urethral strictures, enlarged prostate, 
vesical and renal calculi, etc. , should be treated surgically. Pyelonephritis 
and pyonephrosis also usually require surgical intervention. 



PERINEPHRITIS AND PARANEPHRITIS. 

(Perinephritic Abscess.) 

Etiology. — Inflammation of the fibrous capsule of the kidney (peri- 
nephritis) and of the surrounding flbro-adipose tissue (paranephritis) 
may be due to trauma; to extension of inflammation from the kidney 
(pyelitis, pyelonephritis, pyelonephrosis), from the intestine (especially 
appendicitis and ulcerative processes involving the colon), from the 
vertebrae (tuberculosis), pleura (empyema), etc.; and occasionally 
it follows infections, septicopyemia, etc., the process being embolic. 
The disorder is most common in male adults. 

Pathology. — In some cases the lesions are those of more or less well- 
marked inflammation with considerable inflammatory oedema; the 
process may subside. Usually, however, the lesions progress to suppu- 
ration, the kidney being more or less surrounded with pus, sometimes 
embedded in a large abscess cavity; the pus may have a fecal odor 
(intestinal origin). The abscess may burrow downward along the 
psoas muscle and appear in the groin, or upward into the pleura and 
lungs, and perhaps be evacuated through a bronchus; or it may perforate 
the intestine, the peritoneum, the vagina, etc. Rarely there is a chronic 
indurative perinephritis, thickening and induration of the perirenal 
fibro-adipose tissue, and compression of the kidney (which produces 
no significant symptoms). 

Symptoms. — In the absence of suppuration there are no unequivocal 
symptoms. The phenomena of abscess formation may be insidious 
or abrupt in onset. In the course of one of the aforementioned etiological 
disorders, deep-seated pain develops in the renal region; the pain may 
radiate to the thigh or the testicle (which may be retracted), or be referred 
to or near the hip- joint; the thigh may be favored or flexed (irritation 
of the psoas muscle), and the spine may be immobile from contraction 
of the erector spinse and other muscles of the affected side. On palpa- 
tion there may be swelling of the lumbar region, with perhaps oedema 
of the skin (especially significant); or distinct deep-seated fluctuation 
may be elicited. The general signs of suppuration, chills, fever, sweats, 
and leukocytosis, are usually present; the urine may be clear, or reveal 
the evidence of a concomitant (antecedent or sequential) pyelitis or 
pyelonephritis. 

Diagnosis. — The diagnosis, as a rule, is comparatively easy — by attention 
to the antecedent etiological factors and the evidences of suppuration. 

Prognosis. — The prognosis depends upon the primary cause, the 
amount of damage done, and the amenability of the condition to opera- 



H YDRONEPHROSIS 793 

tion. Cure may be effected in some cases by prompt evacuation of the 
abscess, but in some cases prolonged suppuration and consecutive 
amyloid disease, etc., ensue. 

Treatment. — The treatment is essentially surgical. 

HYDRONEPHROSIS. 

Etiology. — Hydronephrosis, a saccular dilatation of the renal pelvis 
and calices, associated with the accumulation of a urinary fluid, may 
be congenital or acquired, and unilateral or bilateral. The congenital 
cases (bilateral. in 65 per cent, of the cases) are due to atresia of the ureter 
near the renopelvic junction, to congenitally displaced kidneys, or to 
anomalous renal bloodvessels compressing the upper part of the ureter. 
The acquired cases are due to traumatic and inflammatory strictures ; 
partial or complete obstruction by a calculus, or fibrinous, or other plug; 
to displacement of the kidney and angulation or twisting of the ureter; 
or to tumors or other lesions compressing the pelvis or the ureter from 
without, or the ureter at its entrance into the bladder. 

Pathology. — The saccular distention varies considerably in different 
cases, and it may be complete or incomplete, or intermittent. The larger 
distentions occur when the obstruction is of slow development, incom- 
plete, and intermittent rather than when rapid and complete; sudden 
and considerable intrapelvic pressure soon overcomes the renal blood 
pressure and inhibits the excretion of urine, whereas slow increase and 
intermittent reduction of the intrapelvic pressure permits of more 
abundant secretion of urine. The kidney and the pelvis and perhaps 
the ureter are more or less enlarged, irregular, saccular; the renal papillae 
are flattened, the calices distended, the renal tissue atrophic and 
sclerosed. In many cases the kidney and the pelvis form a distinct 
cystic tumor with more or less thinned walls. 

Symptoms. — The symptoms vary with the antecedent and associated 
conditions; in some cases they are inconsequential. In uncomplicated 
cases, such as are common in young adults, the symptoms consist of 
periodic attacks of sudden severe abdominal pain usually localized to 
the region of the kidney (upper right or left abdominal quadrant and 
the costovertebral angle posteriorly) and not radiating down the ureter, 
as a rule; these attacks are often associated with nausea and vomiting. 
Often a more or less large, firm, or cystic tumor may be palpable in the 
region of the kidney — which characteristically varies in size from time 
to time (change in posture, etc.), decrease in size being associated with 
an increase in the amount of urine (intermittent hydronephrosis). The 
changes in the urine are variable, and depend more upon associated 
conditions (inflammations, tumors, calculi, etc.) than upon the hydro- 
nephrosis itself. The intermittent passage of a large amount of clear, 
pale urine of low specific gravity is indicative of the intermittent type 
of the disorder. In the bilateral disorder, which is usually more or less 
permanent, the amount of urine may be below normal. 



794 DISEASES OF THE URINARY SYSTEM 

Diagnosis. — The diagnosis in uncomplicated cases is usually easy. 
Other forms of renal and other retroperitoneal tumors must be excluded. 
Pyonephrosis may be excluded by the absence of evidence of septico- 
pyemia, and of pus from the urine (although some pus cells may be 
found microscopically in many cases of hydronephrosis). The acute 
attacks of pain simulate appendicitis, cholelithiasis, and renal calculus; 
ordinarily little difficulty should be experienced in excluding these. 

Prognosis. — The prognosis depends entirely upon the underlying 
condition and its amenability to treatment. 

Treatment. — The treatment is essentially surgical, although if the 
condition occasions little or no distress, operation need not be insisted 
upon. Division of anomalous bloodvessels where they cross and obstruct 
the ureteropelvic junction suffices in some cases to cure the condition; 
in other cases plastic operations on the ureter and pelvis, nephrotomy, 
anchoring a displaced kidney, etc., may be necessary; or complicating 
calculi, tumors, etc., must be removed. 



NEPHROLITHIASIS. 

(Renal Calculus.) 

Etiology. — Renal calculi are most common in adult life (thirtieth to 
sixtieth year); and in males (75 per cent, of the cases). Their forma- 
tion is said to be favored by a sedentary life and by habits in eating and 
drinking that favor the development of gout. Bacterial infection is 
an active factor in many cases. 

Pathology. — Primarily urinary calculi are renal in origin in the very 
great majority of cases; but secondary accretions may occur in the renal 
pelvis, in the ureter, or in the bladder, and calculous deposits may 
occur in and about divers inflammatory and necrotic processes in the 
urinary tract — whence a distinction is sometimes made between primary 
and secondary calculi. Furthermore, calculi may be solitary or multiple, 
and unilateral or bilateral (20 to 25 per cent, of the cases). According 
to size one may distinguish: (1) Renal sand, fine, gritty particles; 

(2) gravel, concretions up to 1 to 2 mm. in diameter; and (3) calculi 
(or stones), varying in size from that of a pea or bean to large dendritic 
or coral-shaped formations that fill out even a dilated renal pelvis and 
the calices. Chemically the calculi may be composed of: (1) Uric acid 
and urates — the most common (two-thirds of the cases). Sand and 
gravel almost always consist of uric acid and urates; often also the 
small solitary or the larger dendritic stones. These are hard, reddish 
in color, have a smooth surface, and on section are dense and stratified; 
and they occur in acid urine. (2) Calcium oxalate (mulberry calculi, the 
second in point of frequency), hard, gray or dark in color, and with a 
rough surface, or studded with spines; they also occur in acid urine. 

(3) Phosphates (calcium and ammonio-magnesium), small, grayish 
in color, and soft; they are uncommon, and occur in alkaline urine; 



NEPHROLITHIASIS 795 

phosphates may form a coating of other calculi. (4) Certain rarer forms, 
such as calcium carbonate, xanthin, cystin, indigo, and urostealiths 
(fatty calculi, which originate usually in the bladder). Precipitation 
of the urinary salts may occur in the kidney substance — so-called renal 
infarcts, of which the following varieties may be distinguished: (1) 
Uric-acid (urate) infarcts, which occur in the newborn and in gouty sub- 
jects, usually at the apices of the pyramids; (2) calcium (phosphate and 
carbonate, perhaps also oxalate), whitish opaque streaks, found especially 
in the pyramids, in senility, metallic poisoning, etc.; (3) pigmentary 
infarcts — derivatives of hemoglobin, biliary pigment, etc. 

Calculi induce various lesions in the urinary tract. In some (aseptic) 
cases there may be few if any lesions beyond the mere presence of the 
calculus; in other (also aseptic) cases there may be more or less hydro- 
nephrosis or chronic interstitial connective-tissue overgrowth with con- 
traction and atrophy of the renal parenchyma. In infected cases there 
is an associated pyelitis, pyelonephritis, pyonephrosis, or perinephritic or 
paranephritic abscess. In unilateral aseptic cases there may be more 
or less hypertrophy of the opposite kidney; in infected cases there is 
often a descending-ascending infection of the bladder and the other 
kidney. 

The mode of formation of renal calculi is not thoroughly understood. 
Roberts believes that the main factors in the formation of uric acid 
salts are high urinary acidity (which favors the deposition of uric acid), 
excess of uric acid, and deficiency of salines and of pigments. Ebstein has 
proved that urinary calculi are not simple conglomerations of crystalline 
deposits, but that they possess an organic framework, the product of 
pathological processes in the urinary tract, in which the crystalline 
deposits are embedded and held together. Schade, pointing out the 
fundamental error of believing that the urinary constituents exist in simple 
watery solution, emphasizes the importance of the colloids in maintaining 
solution; he states that when the crystalloids go out of solution they 
take with them colloids (pigment, etc.) and form concretions with a 
complex colloidal stroma, to which is due the well-known insolubility 
of the calculus as compared with a simple crystalline mass of the same 
chemical nature. The special colloid is believed to be fibrin or fibrinogen, 
a product of inflammation; which facts, in connection with the frequency 
of infection of the urinary tract and the finding of bacteria in many 
urinary calculi suggest that urinary calculi, in part at least, are infectious 
or inflammatory in origin (analogous to biliary calculi); in part there 
is perhaps an excess in the urine of the crystalloids in question or a 
lessened ability of the urine to hold them in solution. 

Symptoms. — Nephrolithiasis may be entirely latent; a large dendritic 
calculus may constitute an accidental necropsy finding; or sand or 
gravel may be passed from time to time for years with little or no note- 
worthy discomfort; or oliguria or anuria may suddenly develop from 
ureteral obstruction; or such may be the destruction of renal tissue 
that uremia may come on without obtrusive antecedent symptoms. 



796 DISEASES OF THE URINARY SYSTEM 

In the majority of cases, however, the disorder is manifest by renal 
pain, hematuria, pyuria, and other evidences of pyelitis or pyelonephritis. 
The pain may be dull and aching in character in the region of the kid- 
ney, and more or less continuous, although aggravated by violent exer- 
cise (jumping, etc.); or it may be that spoken of as renal colic — sudden 
severe cutting or stabbing pain in the region of one kidney radiating 
down the ureter to the bladder, testicle (which may become retracted), 
urethra, labia, or thigh; rarely to the opposite kidney or upward or 
about the chest. The severe pain is usually associated with strangury, 
reflex nausea, vomiting, and more or less shock (pallor, sweating, and 
feeble rapid pulse); and in children perhaps convulsions. The pain 
may last a few moments and then intermit or remit; or it may recur 
paroxysmally for several hours, the patient perhaps meanwhile being 
conscious of the transit of the calculus through the ureter. Finally, 
it may pass into the bladder and be discharged with the urine (with or 
without a painful paroxysm) ; or it may remain in the bladder and form 
the nucleus of a urinary calculus. Some dull aching usually remains 
for some time after the colic; and the colic may recur from time to time. 
Hematuria is very common; it occurs during and after an attack of colic, 
but it is usually present also in the absence of colic. Pyuria occurs in 
the event of pyelitis and pyelonephritis (which are common). There 
is also albuminuria (proportionate to the pus and blood), crystals of 
uric acid, calcium oxalate, etc. (that sometimes indicate the chemical 
constitution of the calculus); and sometimes also casts (concomitant 
nephritis). Anuria is sometimes observed; it may be due to bilateral 
calculi; to obstruction of one ureter and disease (atrophy) or reflex sup- 
pression of the function of the opposite kidney; or to urethral obstruction. 
In some cases, when the ureter is completely blocked and the opposite 
kidney healthy, the urine voided (excreted by the healthy kidney) may 
be entirely normal. Occasionally there is fever and other septicopyemic 
manifestations of pyelitis and pyelonephritis; in some cases there are 
recurrent attacks which recall Charcot's- biliary intermittent fever (of 
cholelithiasis). The kidney may be tender to palpation, or enlarged 
(hydronephrosis, pyonephrosis). An impacted stone may be palpable 
along the course of the ureter (abdominal or vaginal or rectal palpation). 
An x-tslj examination may reveal the presence, size, shape, and location 
of the stone or stones (uric-acid calculi give a faint shadow; oxalate and 
phosphate calculi, more marked shadows). Cystoscopic examination 
and examination of the separated urines may reveal whether one or 
both sides are diseased. 

A calculus in the bladder gives rise to pain, especially at the end of 
urination, to sudden stoppage of the urinary stream, and to its re- 
establishment upon change of posture (from the erect to the recumbent) ; 
and to hematuria, pyuria, and other evidences of cystitis. It may 
be detected by bimanual and cystoscopic examination of the bladder. 

Diagnosis. — The diagnosis of renal calculus is obvious in the event of 
renal colic, enlargement and tenderness of the kidney, hematuria, pyuria, 



CYSTS OF THE KIDNEY 797 

positive results of an x-ray examination, and the detection of gravel 
or sand; but a negative radiogram by no means excludes a stone. One 
must exclude other causes of pyelitis and pyelonephritis, renal tumors, 
tuberculosis of the urinary tract, essential renal hematuria; and renal 
colic must be distinguished from intestinal and gallstone colic, appendi- 
citis, Dietl's crises, etc. 

Prognosis. — The course is chronic and seldom (but sometimes) results 
in spontaneous cure after the passage of the then existing calculi. The 
likely complications (pyelitis, pyelonephritis) and the likelihood of 
recurrence render the prognosis doubtful. 

Treatment. — Perhaps the dietetic regulations recommended in con- 
nection with gout may tend to prevent the formation of renal calculi. 
The treatment of renal colic is similar to that of gallstone colic — 
rest; morphine, atropine, and perhaps nitroglycerin hypodermicly; 
inhalation of chloroform, if necessary, until the morphine produces its 
effect; a hot foot bath, and hot applications locally. Inversion of the 
patient or the lateral posture sometimes serves to dislodge an impacted 
stone, and reverse massage may lead to the same result. Between 
attacks the patient should avoid sudden exertions. He should keep up 
a goodly excretion of urine by drinking large amounts of water; and in 
the event of uric acid calculi, he should reduce the urinary acidity with 
potassium citrate, acetate, or bicarbonate, etc. (or the alkaline mineral 
waters if desired); in the event of alkaline urine and phosphatic calculi, 
hexamethylenamin, salol, and other urinary antiseptics should be given. 
It seems quite impossible to dissolve calculi in the urinary tract, so that 
it is more than doubtful that lithium salts, piperazin, and other so-called 
uric-acid solvents have any such action in the body. In the event of 
repeated renal colic, pyelitis, anuria, etc., operation should be resorted 
to; and with a full knowledge of the condition, operation should not be 
too long delayed : sooner or later the renal tissue becomes destroyed and 
operation cannot restore it. 

CYSTS OF THE KIDNEY. 

Various sorts of cysts are encountered in the kidneys: (1) Small 
multiple cysts common in chronic indurative nephritis and attributed 
to obstruction and consequent dilatation of renal tubules or Bowman's 
capsules; (2) a large, often solitary cyst, sometimes found projecting 
from the cortex of an otherwise healthy kidney, containing clear watery 
or colloid fluid, and attributable also to obstruction of the tubules (perhaps 
a foetal defect); (3) parasitic (echinococcic) cysts, which cause enlarge- 
ment of the kidney, fluctuation, hematuria, pyuria, and, should the cyst 
rupture into the renal pelvis, vesicles, hooklets, or membrane in the urine 
(the passage of which may occasion renal colic) ; and (4) so-called con- 
genital cystic kidneys. 

Congenital cystic kidneys may be observed at birth (obstructing 
labor) or in later life; many cases first come to observation in adult 



798 DISEASES OF THE URINARY SYSTEM 

life, and especially in men. The kidney may attain an enormous size, 
being made up of numerous cysts, varying in size, as a rule, from 2 to 
20 mm. in diameter, and containing urinous, colloid, or hemorrhagic 
fluid ; often little if any renal tissue can be detected even microscopically. 
The condition is bilateral, although one kidney may be larger than the 
other, and perhaps enlarge before the other. The nature of the disorder 
is not definitely determined; it seems, however, to be a congenital defect 
of development (rather than retention cysts or cystic tumor formation, 
as has been suggested), since it is often associated with other anomalies of 
development), cystic disease of the liver, imperforate anus, malformation 
of the heart, etc.). The condition may remain latent until adult life, 
or, as seems to have occurred in some cases, slow progressive growth 
occurs from early life. In some cases there are the cardiovascular changes 
of chronic indurative nephritis. 

Symptoms. — In some cases the enlarged kidneys interfere with parturi- 
tion. In the cases that develop in later life there are : gradual enlargement 
of both kidneys (although one may precede), which may form visible 
and palpable (perhaps cystic) tumor masses; hematuria — chronic and 
remittent and induced by palpating the kidneys; and the gradual de- 
velopment of the urinary and cardiovascular changes of chronic indura- 
tive nephritis, and of x chronic uremia; sometimes the sudden onset of 
acute uremia. Modern tests reveal lessening of the functional capacity 
of one or both kidneys. 

Diagnosis. — The diagnosis can be readily made in the event of palpably 
enlarged kidneys, hematuria, and the urinary and cardiovascular changes 
of chronic indurative nephritis. 

Prognosis. — The ultimate outlook is hopeless, although the subject 
may live many years (as in chronic indurative nephritis). 

Treatment. — The treatment is that of chronic indurative nephritis. 
Operation may be undertaken in the rare unilateral cases in which the 
other kidney is of good functional capacity (modern tests), and in the 
event of suppuration; but the mortality is high and the outlook not 
reassuring. 

TUMORS OF THE KIDNEY. 

Tumors of the kidney may be benign or malignant, primary or second- 
ary. The benign growths comprise fibroma, lipoma, angioma, and 
adenoma, and are of little clinical interest. The primary malignant 
growths comprise hypernephroma, sarcoma, and carcinoma. The hy- 
pernephroma, a tumor derived from misplaced adrenal tissue, is the 
most common tumor in adults, and includes most of the so-called 
adenomas, carcinomas, sarcomas, endotheliomas, and peritheliomas oc- 
curring in adult life. It may be small and an accidental finding at the 
necropsy, or it may attain the dimension of a man's head. In its early 
growth it is usually encapsulated against the renal substance; but later 
the capsule becomes invaded and penetrated, and the renal veins are 



TUMORS OF THE BLADDER 799 

likely to be implicated — whence metastases occur by way of the blood- 
vessels, to the lungs, bones, etc. Sarcoma is the common tumor in 
infants and children, and may attain a very large size; it may be of 
the common types, but especially when occurring very early in life 
a rhabdomyoma, or a so-called congenital adenosarcoma, etc. Secondary 
tumors may occur by hematogenous or lymphogenous metastases or by 
growth by contiguity of tissue. 

Symptoms. — The significant symptoms consist of pain, hematuria, 
a palpable tumor, and progressive anemia, cachexia, and emaciation. 
The pain may be slight, perhaps absent, or very severe; sometimes it is 
colicky (passage of blood clots down the ureter). Hematuria may be 
mild or severe, continuous or intermittent; it is present sometimes dur- 
ing the course of 50 to 90 per cent, of the cases, but in the early stages 
of hypernephromas it is usually wanting because of the encapsulation 
of the growth and its virtual separation from the kidney tissue. Sooner 
or later a tumor becomes palpable in the renal region retroperitoneally 
(behind the intestines and projecting into the flank or lumbar region); 
it varies in size, is soft or firm, and often nodular. In addition to blood, 
fluid or clotted (casts of the renal pelvis or ureter), the urine may contain 
bits of tumor tissue. Metastasis, especially in adults, to the lungs or 
bones may be observed in some cases; or growth of the tumor may lead 
to thrombosis of the inferior vena cava and oedema of the legs, varicocele 
(compression of the spermatic vein), or to compression and obstruction 
of the intestines, etc. 

Diagnosis. — The diagnosis virtually is that of a retroperitoneal growth, 
in which event hematuria suggests its renal origin; progressive anemia 
and cachexia exclude other enlargements of the kidney (hydronephrosis, 
cystic disease), and the absence of fever and other evidences of septico- 
pyemia excluded pyelonephrosis. Sarcoma of the retroperitoneum 
(Lobstein's cancer) must be excluded. Occasionally also tumors of the 
spleen or the liver must be differentiated. 

Prognosis. — The prognosis depends entirely upon the possibility of 
removal of the growth. 

Treatment. — The treatment is wholly surgical — removal of the tumor. 



TUMORS OF THE BLADDER. 

Tumors of the bladder comprise especially papilloma and car- 
cinoma; fibroma and sarcoma are rare. The major symptoms of 
papilloma or carcinoma consist of local pain, disturbances in urination, 
hematuria, cystitis, and gradually developing anemia and cachexia. 
Sometimes the disorder is not suspected until a small bit of tumor tissue 
is discharged with the urine, whereupon microscopic examination reveals 
the true nature of the disease. In any case the diagnosis may be readily 
made by cystoscopic examination. The treatment is wholly surgical. 



SECTION X. 
DISEASES OF THE NERVOUS SYSTEM. 



Pathological Physiology. — The nervous system, composed of two parts, 
the cerebrospinal and the sympathetic, is the chief regulating and gov- 
erning mechanism of the organism. It is designed to exercise an orderly 
control over all the functions of the body — motor, sensory, secretory, 
vasomotor, and trophic; voluntary and involuntary; conscious and un- 
conscious. The integrity of the nervous system is essential to the proper 
execution of purposeful acts; to muscular activity and coordination; to 
the reception of sensory impressions and the reaction thereto, as in reflex 
action, for instance; to the normal functioning of the special sense organs, 
and of the various glands; to proper growth and trophic influence; and 
to the normal activity of the cardiovascular, respiratory, digestive, uri- 
nary, cutaneous, and reproductive organs. Disorder of the nervous 
system thus becomes manifest not only in morbid phenomena referable 
directly to the system itself, but also in many varied disorders referable 
to the different systems of organs — which have already been discussed. 

In the final analysis the nervous system is made up of a complex of 
neurons; that is, of certain ultimate anatomical and physiological units, 
each of which consists of a cell body, provided with a number of usually 
short, branching processes, so-called dendrons (dendrites), and a single, 
usually long, branch or process, the axon, axis cylinder, or nerve fiber. 
The axons of the cerebrospinal system soon after leaving the cell body 
become ensheathed with myelin and neurilemma (sheath of Schwann), 
both of which are lost near the termination of the axon; these medullary 
sheaths are absent in the sympathetic nervous system. The neurons are 
in physiological relationship or communication by means of so-called 
collateral branches or the terminal arborization of the axon of one 
neuron and the dendrons of another neuron. The prevailing conception 
is that there is no anatomical connection between physiologically related 
neurons, that the relationship is one of contact only — contiguity, but 
not continuity, of structure; but it is not impossible that the ultimate 
divisions of the terminal arborization of the axons actually enter the 
dendrons of another neuron (by means of so-called neurofibrils). 

Neurons are classified as: (1) Primary neurons, which comprise those 
the cell body of which is situated in the central nervous system or ganglia, 
51 



802 DISEASES OF THE NERVOUS SYSTEM 

and the axon of which extends to the periphery (skin, a muscle, a gland, 
a sense organ, etc.); and (2) secondary (or association) neurons, which 
comprise those the cell body of which is situated in the central nervous 
system and the axons of which do not extend to the periphery, but serve 
as a means of communication between different parts of the nervous sys- 
tem; that is, the axon communicates with the dendrons of another 
neuron (primary or secondary). Neurons also are classified, according 
to their function, into motor, sensory, secretory, and trophic; and a 
number of neurons, usually related functionally, are collected and held 
together by neuroglia and other connective tissue, and thus make up the 
different peripheral nerves, the nerve tracts of the spinal cord and brain, 
and the elements of the sympathetic system. Extensive communications 
exist between the cerebrospinal and the sympathetic systems — by way of 
the spinal roots and nerves with the spinal cord, and by way of the vagus 
(chiefly) with the brain. The sympathetic system is largely concerned 
with regulating the cardiovascular system and the vegetative functions; 
its activities are automatic and unconscious, although it is somewhat 
under the influence of the cerebrospinal system, and it may be deranged 
by emotional and other states ; but we know comparatively little of the 
pathology of its disorders. 

All disease of the nervous system is attributed to some disorder of the 
neuron. This may be supposedly functional in nature and temporary 
(functional disorders), or it may be organic, more or less destructive in 
nature, and susceptible of partial or complete repair (organic disease). 
The important facts are that when diseased the neuron is disordered 
(degenerates) as a whole; that many diseases of the nervous system tend 
to involve certain collections of neurons physiologically homologous (so- 
called system diseases); and that a knowledge of the anatomical and 
physiological relationships of these collections of neurons facilitates a com- 
prehension of their diseases and permits a ready localization of the lesion. 

Motor Neurons. — Motor impulses are conveyed from the cerebral 
cortex to the periphery by the motor neurons, of which there are two sets, 
the upper and the lower. The upper motor neuron (the motor tract) 
begins with the cell bodies in the motor area of the cerebral cortex; 
thence the axons pass through the corona radiata, the internal capsule, the 
crus, the pons, the medulla, and the spinal cord. In the pons and 
medulla most of the axons decussate, some to go to the nuclei of the motor 
cranial nerves, the others to course down the opposite side of the spinal 
cord, as the crossed pyramidal tract, and finally to break up into terminal 
arborizations about the cells of the anterior cornua (the cell bodies of the 
lower motor neuron); the axons that do not decussate in the medulla 
descend in the spinal cord as the direct pyramidal tract, but finally also 
decussate to the opposite side by way of the anterior commissure. The 
lower motor neuron begins with the cell bodies in the anterior cornua of 
the spinal cord; thence the axons, by way of the anterior (ventral) spinal 
roots become collected into the spinal nerves, and ultimately reach the 
muscles to which they transmit motor impulses. 



PLATE I 




\reas of Anaesthesia upon the Body after Lesions in the Various 
Segments of the Spinal Cord. 

The segments of the cord are numbered: C I to VIII, D I to XII, L I to V, S 1 i . r >, 
Hand these numbers are placed on the region of the skin supplied by the sensory nerves of 
Hthe corresponding segment. 



PATHOLOGICAL PHYSIOLOGY 803 

Motor impulses must pass through both of these neurons; and disease 
of one or the other or both results in loss of voluntary muscular power. 
There are, however, differences in the other results of disease of the two 
motor neurons, which are due to the fact that the upper neuron exercises 
an inhibiting influence on the lower, and that the lower serves to main- 
tain the nutrition of the muscles with which it is connected. In general, 
therefore, disease of the upper motor neuron results in loss of voluntary 
muscular power, rigidity and spasticity of the muscles, and eventual 
contractures (the muscles of flexion and adduction overcoming those of 
extension and abduction); increase of the deep reflexes, as well as the 
Babinski plantar reflex (extension of the great toe) ; little if any muscular 
wasting, and that only from disuse; and no noteworthy changes in the 
electrical reactions of the nerves or muscles. This is well exemplified 
in lateral sclerosis (spastic paraplegia) and in combined lateral and pos- 
terior sclerosis (ataxic paraplegia). On the other hand, disease of the 
lower motor neuron results in loss of. voluntary muscular power, flac- 
cidity, and wasting of the muscles; ultimate contractures, due largely 
to the action of unopposed non-paralyzed muscles; loss of deep reflexes; 
and often the response to electrical stimulation known as the reactions of 
degeneration. This is well exemplified in epidemic poliomyelitis (in- 
fantile paralysis), progressive spinal muscular atrophy, progressive bul- 
bar paralysis, etc. In some cases both motor neurons may be diseased, 
as in amyotrophic lateral sclerosis. 

Sensory Neuron. — Sensory impressions are conveyed from the 
periphery to the nerve centres by the sensory neurons. The cell bodies 
of these are situated in the ganglia of the posterior spinal roots and in the 
homologous ganglia of the sensory cranial nerves, as well as in the sym- 
pathetic nervous system. The sensory impression is received by certain 
fine nerve filaments in the skin or tactile corpuscles and conveyed by a 
sensory nerve or bundle (through or past the cell body) to the spinal 
cord. Herein the axon bifurcates, one portion ascending in the posterior 
columns, the other descending a short distance. 

The peripheral nerves carry three systems of sensory fibers: (1) The 
protopathic system, which transmits sensations of pain and of extremes 
of temperature (above 45° C. and below 20° C.) ; (2) the epicritic system, 
which transmits sensations of light, touch, of cutaneous localization, and 
of slight temperature variations; and (3) the deep sensibility system, 
which transmits sensations of pressure and of movements of the joints, 
muscles, and tendons — so-called muscle sense (the ability to distinguish 
difference in weight of objects of similar size), as well as the stereognostic 
sense (the ability to recognize the shape of objects), and the ability to 
recognize with the eyes closed the position into which the limbs may be 
passively placed. The unit of the protopathic system is in the posterior 
spinal roots, that of the epicritic system in the peripheral nerves; so that 
the areas of sensory disturbances are different in disease of the periph- 
eral nerves (Fig. 15) from what they are in disease of the spinal roots or 
segments (Plate I). Furthermore, after injury to a peripheral nerve, for 



Fig. 15 




Great -«P*«»,.r-7 
lumcular:*" •^Uental 

'■^Superficial j 
\ Cervical 



/Acromial Sternal-, 

'branchy Middle branch.- 

i branch ..-■■"" 




Inf. Hemorrhoidal 

ofPudic 

Superficial Perineal o 

Pudic and Inferior 

Pudendal of small 

Sciatic 




The distribution of the sensory nerves in the skin. The areas of the skin supplied by the 
cutaneous nerves are shown in finely dotted outline. The circles on the trunk show areas occa- 
sionally anesthetic in hysteria. The lines across the limbs at the ankle, knee, thigh, wrist, 
elbow, and shoulder show the upper limits of anesthesia in multiple neuritis of varying degrees 
of severity. (After Flower.) 



PLATE II 




XIII 



The Cervical and Sacral Enlargements of the Spinal Cord in Cross-section. 

(Starr.) 

Showing the various neurons in the gray matter, the direction of their axons, and the 
varieties of fibers in the different columns of the cord. Blue, motor neurons ; red, sensory- 
neurons ; purple, association neurons and axons. 

I. Ant. median column. II. Anterolateral column. III. Gowers* anterolateral ascending column. 
IV. Marginal column. V. Lateral pyramidal column. VI. Direct cerebellar column. VII. Lissauer's 
tract. Vin. Ext. portion of column of Burdach. IX. Root zone of the column of Burdach. X. 
Descending comma-shaped bundle of Schultze. XI. Post, commissural tract. XII. Column of Goll. 
XIII. Septomarginal tract. 



PATHOLOGICAL PHYSIOLOGY 805 

instance, the different forms of anesthesia are not alike in distribution, 
and during recovery the sensibility to pain returns before that of mere 
touch; that is, sensation for touch and pain is subserved by different 
fibers. If a peripheral nerve represents largely a single posterior spinal 
root, the area of analgesia is likely to be well defined; but if the peripheral 
nerve contains fibers from several posterior spinal roots, the disturbances 
of protopathic sensibility are likely not to be well demarcated. After all 
the cutaneous sensory fibers have been destroyed, the deep sensibility of 
the part may still be preserved. 

Sensory impressions are transmitted in the spinal cord by the following 
tracts (Plate II) : (1) The posterior columns — the postero-internal column 
of Goll, and the postero-external column of Burdach. The fibers of these 
columns are a continuation of those of the posterior roots; they ascend, 
giving off collateral branches which penetrate the gray matter of the cord, 
and they terminate in the homolateral nucleus gracilis and nucleus cune- 
atus of the medulla; thence another set of fibers proceeds, soon decus- 
sates, and ends in the thalamus of the opposite side; from this, in turn, 
another set of fibers proceeds to the sensory area of the cerebral cortex. 
These fibers are chiefly concerned in transmitting impulses of cutaneous 
tactile sensibility (light touch) and localization, and of deep sensibility, 
especially muscular and limb position; lesions of these fibers give rise 
to ataxia. A few fibers cross soon after they enter the cord, ascend in 
contralateral ascending anterior column, and finally terminate in the 
thalamus. These fibers also transmit impulses for tactile sensibility, and 
may escape involvement in cases of Brown-Sequard paralysis. The 
posterior columns also contain fibers concerned in the transmission of 
painful impressions; soon after entering the cord they terminate about 
cells in the gray matter, whence other axons proceed, decussate, and 
ascend in the opposite anterolateral tract. (2) The anterolateral tract 
of Gowers. This comprises the aforementioned fibers for pain, as well 
as others concerned in transmitting temperature impulses; these ulti- 
mately, in large part, reach the cerebellum, by way of the superior ped- 
icle), but some of them proceed to the homolateral thalamus. (3) The 
direct (dorsolateral) cerebellar tract of Flechsig. Some of the fibers 
entering the cord by way of the posterior roots, proceed to cells in Clark's 
columns (at the base of the posterior cornua); thence axons proceed, 
ascend as the direct cerebellar tract, and end in the cerebellum. These 
fibers convey impulses of deep sensibility (muscles, joints, tendons, etc.), 
and disorder of them results in ataxia. 

Reflexes. — The contraction of a muscle or set of muscles that fol- 
lows a sensory impulse is known as a reflex act; its occurrence is depend- 
ent upon the integrity of the so-called reflex arc. This is composed of 
(a) an afferent (sensory) nerve, along which the impulse passes, enters 
the spinal cord by way of the posterior roots, and reaches (b) the 
so-called centre, the motor cells of the anterior cornua; from these, in 
response to the stimulus, an impulse passes out along (c) an efferent 
(motor) nerve, and, reaching a muscle, causes it to contract. Reflexes 



806 DISEASES OF THE NERVOUS SYSTEM 

may occur in the event of integrity of a single segment of the spinal cord; 
but, although independent of, they are much modified by, the higher 
centres in the brain. In disease they may be lessened (or abolished) or 
exaggerated. Lessening or absence of the reflexes implies a lesion in 
either the sensory nerve, in which event it is associated with anesthesia; 
or in the motor cells in the anterior cornua, or in the motor nerve, in 
which event it is associated with paralysis, flaccidity, and wasting of the 
muscles; or in the sensory reflex fibers within the spinal cord, in which 
event the reflexes being diminished or absent, without associated sensory 
(anesthetic) or motor (paralytic) phenomena referable to a nerve trunk, 
means a lesion of the spinal cord. Of these, the most important are 
locomotor ataxia, paretic dementia (with associated posterior sclerosis), 
acute and chronic anterior poliomyelitis, syringomyelia, diffuse and 
transverse myelitis, as well as hemorrhage and tumors (which abolish 
reflexes at the level of the lesion), and multiple sclerosis (which also may 
abolish a reflex if a sclerotic patch involves the reflex arc). Exaggeration 
of the reflexes occurs in consequence of lessening or abolition of the in- 
hibiting influence of impulses normally passing from the brain by way of 
the motor tracts in the lateral columns of the spinal cord; the exaggera- 
tion may progress to the condition known as clonus, which comprises a 
series of rapidly recurring contractions of a muscle, provoked by sudden 
marked tension on the tendon of the muscle. Exaggerated reflexes are 
indicative of disease of the lateral columns of the spinal cord, and are 
found especially in lateral sclerosis (spastic paraplegia), below the lesion 
in cases of descending degeneration of the pyramidal tracts, in the early 
stages of amyotrophic lateral sclerosis (later they become lost in the 
arms), in conditions of slight pressure impeding the passage of inhibiting 
impulses down the cord (as in the early stage of caries of the vertebra?, 
tumors, etc., causing slight compression), and in functional disorders, 
such as hysteria and neurasthenia. In cases of complete severance of 
the cord, however, the reflexes are abolished below the lesion. 

There are three principal classes of reflexes: (1) The deep or tendon 
reflexes, which result from tapping a tendon near its insertion, whence 
contraction of the muscle ensues. The most important are the knee- 
jerk (patella tendon reflex), the Achilles tendon reflex, the biceps, the 
triceps, the supinator longus, the plantar (flexion) tendon reflex, etc. 
Special diagnostic importance attaches to the knee-jerk: it may be 
diminished or lost in disturbance of the reflex arc interfering with the 
transmission of impulses, such as disease of the muscles, nerves (neu- 
ritis), posterior roots (tabes dorsalis), or anterior roots, and disorders of 
the lumbar cord (second, third, and fourth lumbar roots) which destroy 
the centre (acute and chronic poliomyelitis, etc.). In some cases, occa- 
sionally, but only for a very short time, the knee-jerks may also be lost — 
from irritation or stimulation of the inhibiting influence of the pyramidal 
fibers — in cerebral hemorrhage, meningitis, compression of the cord from 
fracture-dislocation, etc. The knee-jerks may be exaggerated in conse- 
quence of lessening or abolition of the inhibiting influence of the pyram- 



PATHOLOGICAL PHYSIOLOGY 807 

idal tract above the lumbar region, such as occurs in lateral sclerosis 
(spastic paraplegia), transverse myelitis, compression from fracture- 
dislocation or other causes (except in cases of complete severance of the 
cord, in which event the reflexes below the lesion are abolished); exag- 
geration of the knee-jerk occurs also in functional disorders, such as 
hysteria and neurasthenia. Under like conditions, exaggeration of the 
Achilles tendon reflex — that is, ankle clonus — may ensue, and the so- 
called Babinski phenomenon (or sign) may be elicited; this, which con- 
sists of extension (sometimes called dorsal flexion) of the great toe upon 
stimulating the sole of the foot, is proof of disease of the upper motor 
neuron. (2) The superficial or cutaneous reflexes, which are elicited 
by stroking or irritating the skin. The most important are the epigastric 
reflex — contraction of the muscles of the epigastrium upon stroking the 
lower part of the thorax; the cremasteric reflex — retraction of the testicle 
and scrotum upon stroking the inner aspect of the thigh; the gluteal 
reflex — contraction of the gluteus muscle (dimpling in the gluteal 
fold) on stroking the buttock; and the abdominal, scapular, palatal, 
pharyngeal, and conjunctival reflexes. Most of these reflexes are 
believed to be due to contraction of involuntary muscular fibers beneath 
the skin near the point of irritation. The presence of these superficial 
reflexes implies integrity of the reflex arc, whence they may serve to deter- 
mine the level of disease of the spinal cord. In general they are dimin- 
ished or absent in diseases in which the deep or tendon reflexes are exag- 
gerated. (3) Visceral reflexes, of which the most important are: (a) 
pharyngeal and laryngeal reflexes, which, when lessened or abolished, 
result in difficulty in swallowing and coughing, and may lead to regurgi- 
tation of food through the nose, or to aspiration pneumonia or asphyxia- 
tion; (b) visceral and rectal reflexes. Disease of the spinal cord above 
the centre for the bladder and the rectum (fourth and fifth sacral segments) 
results in loss of control by higher centres, so that the bladder must 
depend upon its reflex activity; usually it becomes overdistended and 
finally overflow from distention ensues. If the spinal centres are de- 
stroyed retention of urine is usually impossible, and there is continuous 
incontinence. The result of involvement of the rectal centre is consti- 
pation and involuntary evacuation of the feces. 

Electrical Reactions.— Normally the application of a faradic (in- 
terrupted) or galvanic (constant) current to a nerve or muscle results in 
contraction of the muscle, especially when the current is applied to the 
so-called motor points. On the use of the galvanic current, contractions 
occur only when the contact is made or broken; and normally the 
cathodal (negative pole) closing contraction (CCC) is greater than the 
anodal (positive pole) closing contraction (ACC). In lesions of the lower 
motor neuron, usually within four or five days, the so-called reactions of 
degeneration develop. The nerve shows a gradual loss of excitability to 
both the faradic and the galvanic currents, and finally fails to respond at 
all, that is, there is no muscular contraction upon applying the current 
to the nerve. The muscle at first responds feebly and slowly to the 



808 DISEASES OF THE NERVES 

faradic current, but soon ceases to respond; on the other hand, the 
muscle may be for some time unduly sensitive to the galvanic current, 
that is, it may respond to a weaker current than in health; but the char- 
acteristic reactions of degeneration consist in a slow, wave-like contrac- 
tion to the galvanic current (instead of instant and quick response, as in 
health), and in the anode-closing contraction being greater than the 
cathode-closing contraction. This last is sometimes not present (partial 
reaction of degeneration). In severe cases all response to even the gal- 
vanic current may become lost. A gradual increase in galvanic irrita- 
bility in cases in which it has been absent or slight is of good prognostic 
significance, indicating regeneration. 



DISEASES OF THE NERVES. 



NEURALGIA. 

Neuralgia is a term used to describe recurring or persistent pain in a 
peripheral nerve and its area of distribution. Strictly speaking, the pain 
is unassociated with demonstrable lesions in the nerve trunk or its centres, 
but the pain of definite neuritis is also often spoken of as neuralgia. 

Etiology. — Neuralgia occurs especially in neuropathic individuals or 
families, and is more common in women than in men. It is commonly 
provoked by anemia and general nervous debility; but it may follow 
" taking cold," or be due to infections, such as malaria, typhoid fever, 
rheumatism, etc.; to intoxications, such as intestinal auto-intoxication, 
Bright's disease, gout, etc. ; or to reflex irritation, such as carious teeth, 
eyestrain, etc. 

Pathology. — Neuralgia fer se is not associated with demonstrable ana- 
tomical lesions. The pain is very likely due to irritation or oversuscep- 
tibility of the sensory neuron. 

Symptoms. — The chief symptom is pain. Although this may be more 
or less constant, it is characteristically intermittent, recurring from time 
to time (seconds, minutes, or longer intervals) in paroxysms of sharp, 
stabbing, lightning-like aching or boring pain, which is limited to the 
area of distribution of a nerve or group of nerves. Usually there is also 
hyperesthesia over this area, and painful or tender spots along the course 
of the nerve; and there may be vasomotor alterations, such as pallor or 
flushing, excessive sweating, erythema, or cedema, and trophic changes, 
such as blanching and falling of the hair. Reflex spasms of the muscles 
in the painful area sometimes supervene, as in trigeminal neuralgia. 
The attack may last several minutes, several hours, or a day or more, and 
recur at regular or irregular intervals. 

Trigeminal neuralgia (trifacial neuralgia; tic douloureux), a very 
common disorder, may be symptomatic of carious teeth, eyestrain, nasal 



NEURALGIA 809 

disease, brain tumor, etc., or it may occur as an apparently primary dis- 
order of unknown cause. The pain, which is often extremely severe, 
may be limited to any one of the three great divisions of the nerve (the 
ophthalmic, the superior and the inferior maxillary), but it may involve 
all three; it is rarely, if ever, bilateral. Cutaneous hyperesthesia is 
usually present, painful or tender spots are commonly found where 
the nerve emerges from the foramina, and the eyebrows and the hair 
are likely to become gray or fall out. The paroxysms may be set up 
by various sorts of stimuli, such as a draught of cold air, touching the 
hyperesthetic area, the movements of chewing, speaking, etc. ; they tend 
to increase in severity and the intervals to lessen; and associated spasm 
of the facial muscles may supervene (facial spasm). 

Cervicooccipital neuralgia occurs in the back of the head, in the area of 
distribution of the first four cervical nerves; it may be confined to the 
posterior branches. There is often a tender spot midway between the 
mastoid process and the first cervical vertebra where the great occipital 
nerves emerge, between the trapezius and the sternomastoid muscle, 
and above the parietal eminence. The scalp is usually markedly hyper- 
esthetic. 

Cervicobrachial neuralgia occurs in the shoulder and arm, in the area of 
distribution . of the four lowest cervical and the first thoracic nerves 
(brachial plexus). Tender spots may be found at the posterior border of 
the deltoid muscle (circumflex nerve), over the musculospiral nerve near 
the outer condyle of the humerus, over the ulnar nerve in the groove 
between the inner condyle and the olecranon process, and over the ulnar 
and the radial nerves at the wrist. 

Phrenic neuralgia sometimes follows pleurisy or pericarditis, and only 
very rarely occurs as a primary disorder. The pain occurs at the lower 
part of the chest, in the neighborhood of the attachment of the diaphragm, 
and is aggravated by deep inspiration, coughing, sneezing, and other 
sudden or violent movements of the diaphragm. 

Intercostal neuralgia is very common. The pain follows the course of 
the intercostal nerves, and is often continuous, though subject to acute 
exacerbations. Painful spots are common near the vertebrae, where the 
posterior branches emerge; in the midaxilla, where the lateral branches 
reach the surface; and toward the anterior midline, where the anterior 
branches reach the surface. The most intractable intercostal neuralgia 
(as well as other neuralgias) may follow herpes zoster. 

Lumbar neuralgia occurs in the area of distribution of the sensory 
fibers of the sacral plexus, and is most common along the crest of the 
ilium, in the inguinal region, and in the genitalia (scrotum and labia). 

Coccygodynia, a neuralgia of the coccygeal plexus, is common in 
women. The pain may be more or less constant and intractable, and is 
usually aggravated, or at least induced, by the sitting posture. 

Sciatica may be a neuralgia, although it may result also from neuritis, 
pressure of tumors, enlarged lymph nodes, sacro-iliac disease, etc. The 
pain, which is often severe, may extend throughout the course of the 



810 DISEASES OF THE NERVES 

nerve and into its branches in the leg. Hyperesthesia is usually present, 
and painful spots may be found at the sciatic notch; in the popliteal space, 
and at the outer edge of the fibula. There is usually pain and difficulty in 
walking, and the common attitude in standing and walking (throwing the 
weight on the unaffected side) may lead to lateral curvature of the spine. 

Meralgia paresthetica is a neuralgia (or neuritis) of the external 
cutaneous nerve that gives rise to painful paresthetic phenomena on the 
outer side of the thigh, and sometimes also some anesthesia. 

Plantar neuralgia may occur in the tips of the toes, or it may be more 
widespread. It is rather common in typhoid fever. 

Painful heel (pododynia) may be a pure neuralgia, but in some cases 
it results from definite exostoses and infiltrations of the plantar fascia. 
They are not uncommon after gonococcic infection, and may be demon- 
strated by the arrays. Pains in the feet also are often due to flat foot. 

Metatarsalgia, Morton's painful affection of the foot, is usually attrib- 
uted to compression of the metatarsal nerve (usually about the fourth 
metatarsal phalangeal joint). 

Visceral neuralgias are sometimes described, such as cardialgia, gas- 
tralgia, hepatalgia, nephralgia, etc., but these painful affections usually 
have an anatomical basis. 

Diagnosis. — Neuralgia should be distinguished from definite neuritis. 
In neuralgia there is no discoverable cause for the pain; the pain is usu- 
ally unilateral, corresponds with the area of distribution of a nerve, and 
is characteristically paroxysmal and intermittent; there is no noteworthy 
anesthesia (rather hyperesthesia), no muscular wasting, and no reactions 
of degeneration; in neuritis there is early and usually marked tender- 
ness along the nerve trunks. The pains of tabes dorsalis, of gummas, 
and of inflammation of the meninges should not be mistaken for neuralgia. 

Prognosis. — The neuralgias of general ill health and anemic states 
usually disappear with the causative factors. Trigeminal neuralgia, 
sciatica, and the pain following herpes zoster, etc., may continue for a 
long time — sometimes indefinitely. 

Treatment. — Possible causative factors must be searched for, such as 
carious teeth, refractive errors, nasal disease, pressure of tumors, anemia, 
nervous exhaustion, gout, etc., and, when found, these must be appro- 
priately treated. Iron and arsenic are useful in any event; in some 
cases also phosphorus, cod-liver oil, and strychnine. Quinine is of value 
in cases definitely malarial, and perhaps in some other cases, for its bitter 
tonic properties. The iodides sometimes render service in chronic cases 
and in those associated with arteriosclerosis, gout, etc. Alkalies, such as 
sodium benzoate, ammonium chloride, etc., gelsemium, and cannabis 
indica also have been recommended, as well as injections of alcohol into 
the nerve. Otherwise, the treatment is largely that of pain: hot applica- 
tions, freezing the skin (ether or rigoline spray), the Paquelin cautery, 
blistering, the application of equal parts of camphor, chloral, and menthol, 
and galvanism locally; and the internal use of the coal-tar analgesics 
(acetphenetidin, acetanilide, etc.). These, as well as preparations of 



NEURITIS 811 

opium, should be used with the greatest caution, since the common 
intractability of neuralgia is likely to lead to the formation of a drug 
habit. In many cases surgical treatment must eventually be resorted 
to — resection of the nerve (or of the Gasserian ganglion in trigeminal 
neuralgia). 

NEURITIS. 

Etiology. — Neuritis may be acute or chronic, and it may involve one 
or many nerves — mononeuritis or multiple neuritis. Single or mono- 
neuritis may be due to traumatism, to the action of cold, or to extension 
of inflammation from adjacent parts, as facial neuritis in middle-ear 
disease and caries of the temporal bone. Multiple neuritis may be due 
to infections (diphtheria, typhoid fever, pyococcic infections, leprosy, 
etc.), and those factors associated with "catching cold" and exposure 
(acute febrile polyneuritis); exogenous intoxications, such as alcohol, 
lead, arsenic, and mercury, and that associated with beri-beri; endog- 
enous intoxications associated with gout, diabetes, nephritis, intestinal 
auto-intoxications, etc. ; anemic and cachectic states. 

Pathology.— In general the lesions are those of inflammation (conges- 
tion, oedema, and cellular infiltration), fragmentation of the myelin 
sheaths, and parenchymatous swelling and ultimate fatty and granular 
degeneration of the nerve fibers. The lesions may be superficial, chiefly 
perineural, or they may penetrate to the deeper parts- — so-called inter- 
stitial neuritis. In some cases (so-called parenchymatous neuritis) the 
axons are chiefly involved, showing degenerative changes alike to those 
that follow isolation of the axon from the cell body. The cell bodies also 
may reveal changes showing that the etiological factor tends to involve 
the entire lower motor neuron. 

Symptoms. — Since most of the peripheral nerves carry motor, sensory, 
and trophic fibers, the symptoms of neuritis may be also motor, sensory, 
and trophic. In single or mononeuritis the chief complaint is usually 
of pain in the course of the nerve and in its area of distribution. In 
addition there is usually hyperesthesia and perhaps hyperalgesia or 
paresthesia of the overlying skin; in some cases also patches of hypesthesia 
or anesthesia, or sometimes erythema or oedema. Furthermore, there is 
loss of power of the muscles, which soon become flabby, wasted, and 
tender (especially on motion or pressure), and reveal fibrillary twitchings 
and the reactions of degeneration. The reflexes become lessened and 
may disappear. The involved nerve, if accessible to palpation, is found 
swollen and tender. In protracted cases, in addition to the foregoing, 
more or less marked trophic changes occur: the skin becomes thin, 
smooth, red, and shiny or glossy; the tips of the fingers become pointed 
(from atrophy also of the subcutaneous tissues) ; the nails and the hair 
grow irregularly; and the joints may become stiff and immobile. 

In multiple neuritis, since the poison is carried by the blood, the lesions 
are widespread and usually symmetrically bilateral. In the acute 



812 DISEASES OF THE NERVES 

febrile (infectious or toxic?) cases the onset, following cold or exposure, 
may be sudden, and attended by a chill or chilliness, fever (103° to 104°), 
pains and tenderness of the limbs, and loss of muscular power. The 
other symptoms mentioned under mononeuritis develop, but are wide- 
spread, and the patient is usually totally incapacitated. 

The alcoholic (the most common) cases usually begin with paresthesia 
(tingling or numbness) and hyperesthesia, especially in the legs, and these 
may be associated with tenderness of the calf muscles. Soon weakness of 
the muscles of the legs, especially of the anterior tibial group, develops; 
this leads to "foot-drop" and to a characteristic high-steppage gait. 
There is also atrophy of the muscles, loss of the knee-jerk and the plantar 
reflex, the reactions of degeneration, incoordination (loss of muscle sense), 
and other phenomena mentioned under mononeuritis. In advanced cases 
walking finally becomes impossible (complete paralysis), and areas of 
anesthesia (stocking-and-glove, or cuff forms) supplant the hyperesthesia. 
The arms maybe involved, but less commonly and less severely. Although 
the cranial nerves usually escape, vision may become impaired, optic 
neuritis may occur, and involvement of the phrenic nerve (paralysis of the 
diaphragm) or of the vagus nerve (tachycardia) may ensue. Mental 
phenomena are not uncommon in aggravated cases, such as loss of mem- 
ory, hallucinations, mental deterioration, and delirium. Some chronic 
alcoholic subjects exhibit the combination of multiple peripheral neuritis, 
loss of memory, and pseudoreminiscences (false notions as to time, 
place, and actualities) — a condition spoken of as Korsakoff's psychosis. 

The arsenical cases much resemble the alcoholic; the legs are usually 
involved first, but the arms may become implicated later, and there is 
usually also a brownish pigmentation of the skin. In the cases due to 
lead the extensors of the wrist and hand are most likely to become in- 
volved (wrist-drop), and the other symptoms mentioned on page 295 
develop. In the diphtheritic cases the muscles of the palate are com- 
monly involved and lead to regurgitation of food through the nose; but 
the external muscles of the eye may become affected or the disorder 
may become widespread. 

Diagnosis. — The diagnosis is usually apparent from the mentioned 
symptoms. The neural distribution of the motor and sensory symp- 
toms, tenderness of the nerve trunks and the muscles, the bilateral 
symmetry of the phenomena in the multiple neuritis cases, and the 
absence of involvement of the sphincters of the bladder and the rectum 
and of the Argyll Robertson pupil usually serve to exclude spinal-cord 
disease. 

Prognosis. — The outlook in general is good, gradual improvement 
occurring in most cases after the lapse of several weeks or months. Re- 
covery, however, may not be complete, and death may ensue from com- 
plications, such as bronchopneumonia. 

Treatment. — The causative factor must first be entirely eliminated — 
especially alcohol, arsenic, lead, gastro-intestinal autotoxemia, etc. Rest 
and good nutritious food are essential in all cases, and care must be 



HERPES ZOSTER 813 

exercised that deformities do not ensue. The initial pains may be re- 
lieved by local applications, such as hot fomentations, saturated solu- 
tions of magnesium sulphate, liniments containing chloroform, bella- 
donna, etc., and by the internal use of salicyl preparations or small 
doses of acetphenatidin and other coal-tar derivatives. After the acute 
manifestations have subsided, resort should be had to massage, passive 
movements, and galvanism to maintain the nutrition of the muscles, and 
the patient should be encouraged to attempt voluntary movements. 
Strychnine in large doses is useful in many cases, and iron, quinine, cod- 
liver oil, and other tonics in the anemic cases. 



HERPES ZOSTER. 

Herpes zoster is an acute, probably specific, infectious inflammation 
and degeneration of the ganglia of the posterior spinal roots and of the 
homologous ganglia of the sensory cranial nerves, characterized clinically 
by fever, and by pain, erythema, and an herpetic eruption in the area of 
distribution of one or more of these roots. 

Etiology. — Head and Campbell seem to have proved that herpes 
zoster is an acute specific infectious disease, involving especially the pos- 
terior spinal roots and ganglia, but the infectious agent has not been deter- 
mined. The disorder also sometimes develops secondarily to tubercu- 
losis of the vertebra?, meningitis, etc. 

Pathology. — The chief lesions consist of inflammatory foci, with ne- 
croses and hemorrhages involving the affected ganglion and its sheath. 
Many ganglion cells are destroyed, and in consequence their axons and 
dendrons in the peripheral nerves and the spinal cord undergo sec- 
ondary atrophy. The disease in many respects is the sensory analogue 
of acute poliomyelitis. The facial herpes of pneumonia and other infec- 
tions is an analogous condition (involvement of the Gasserian ganglion). 

Symptoms. — The onset may be abrupt, with fever, malaise, gastro- 
intestinal disturbances, perhaps enlargement of the lymph nodes, etc. 
Usually on the third or fourth day, and often preceded by pain and ten- 
derness of the skin, an herpetic (or vesicular) eruption breaks out. This 
is most common on the trunk (intercostal nerves) and is usually unilateral ; 
it is confined to the area of distribution of one or more posterior spinal 
roots (segmental distribution), and it is especially characterized by a 
patchy distribution of the vesicles corresponding to the posterior, lateral, 
and anterior division or distribution of the nerves. At the end of a week 
or ten days the vesicles usually dry up. Small depressed scars com- 
monly persist; sometimes also a postherpetic pain and various sensory 
disturbances, and occasionally a most intractable neuralgia. Transient 
motor paralysis may be observed, especially of the muscles of the facial 
nerve innervation in trigeminal or occipito-cervical nerve herpes (com- 
pression of the facial nerve by a swollen geniculate ganglion, Ramsey 
Hunt). 



814 DISEASES OF THE NERVES 

Treatment. — The early pain may be relieved by coal-tar derivatives, 
salicyl preparation, or opium. Zinc stearate or similar dusting powder, 
or a mild antiseptic ointment may be applied locally. Intractable neu- 
ralgia, if not otherwise relieved, may necessitate division of the posterior 
spinal roots involved or removal or isolation of the homologous cranial 
nerve ganglion. 

NEUROMAS. 

Neuromas may be true or false. The true neuroma is a tumor made up 
of nerve fibers, and sometimes also of ganglion cells; it is a rare growth. 
The false neuromas are of divers sorts: (1) Various forms of fibromas, 
myxomas, or sarcomas that may develop from the connective tissues of 
the nerves, and usually give rise to fusiform swellings. (2) The so-called 
amputation neuromas — painful, bulbous enlargements of the ends of 
divided nerves. They are common in stumps after amputations, and 
consist of a mass of axons growing peripherally — supposedly with a view 
to reach their normal endings. (3) Pleociform neuromas — a condition, 
often hereditary and congenital, consisting of multiple fibrous tissue 
growths that may involve almost if not quite all the nerves of the body. 
More than a thousand of these tumors have been found in a single case. 
(4) Generalized neurofibromatosis (yon Recklinghausen's disease), a con- 
dition consisting of: tumors along the nerves akin to those of the plexi- 
form neuroma; various motor and sensory phenomena depending upon 
the situation of these growths; distorted mentality, consisting especially of 
general failure of intellectuality and disorders of speech; soft, sessile, or 
pedunculated growths of the skin (neurofibromatosis of the skin; mol- 
luscum fibrosum; so-called elephantiasis neuromatosa, when of great 
size); and areas of brownish pigmentation of the skin. (5) Tuber cula 
dolorosa, small, painful, multiple neuromas involving the cutaneous ter- 
minations of the sensory nerves, and found especially in the breast, on 
the face, or about the joints. (6) Dejerine's interstitial hypertrophic 
progressive neuritis of childhood (thickening of the nerves, with general 
muscular atrophy and the symptoms of tabes dorsalis; page 856). 



DISEASES OF THE CRANIAL NERVES. 

I. Olfactory Nerve. — The olfactory nerve may become diseased in 
the terminal cells, in the olfactory mucous membrane, in the cells in the 
olfactory bulb, in the olfactory tracts, or in the cortical cells in the unci- 
nate convolution. The disorders consist of : (1) Anosmia or hypoosmia 
(loss of the sense of smell), which may occur in chronic nasal catarrh, 
disease of the bulb or tracts (injuries, meningitis, etc.), central disturb- 
ance, or hysteria (usually unilateral); (2) hyperosmia, which is com- 
monly observed in hysterical and neurasthenic women; and (3) par- 
osmia— perversion or hallucinations of smell— which may occur after 



DISEASES OF THE CRANIAL NERVES 815 

injuries, in tumors of the uncinate convolution, in the insane, and may 
constitute the aura of epilepsy. 

II. Optic Nerve. — Functional Disorders. — Functional disorders of the 
retina are sometimes observed, such as hyperesthesia, which is occa- 
sionally seen in hysterical women and in the early stages of meningitis 
(photophobia) ; night blindness — nyctalopia, good vision in a strong light 
and poor vision in twilight; and hemeralopia, good vision in twilight 
and poor or painful vision in a bright light; hysterical amblyopia or 
amaurosis, which is encountered in hysterical subjects; and toxic 
amblyopia or amaurosis, which may be due to tobacco, lead, quinine, etc. 
In the toxic, especially tobacco, cases there is gradual bilateral impair- 
ment of sight, especially centrally and for colors (central scotoma for red 
and green). In advanced cases a retrobulbar neuritis may ensue, with 
atrophy of the macular bundle and of the disk. 

Neuroretinitis.— Neuroretinitis is common in chronic nephritis, severe 
anemic conditions, and leukemia, and it may be observed also in 
syphilis, malaria, diabetes, lead poisoning, etc. The chief lesions consist 
of hemorrhages and opacities of the retina. The disorder may be well 
advanced before there is any notable impairment of vision. 

Optic Neuritis; Papillitis; Papillcedema ; Choked Disk. — Papilledema is 
sometimes seen in chronic nephritis, severe anemic states, etc.,*in which 
it is usually associated with neuroretinitis; but it is especially significant 
of increased intracranial pressure, and is therefore most common in 
brain tumors (at least 90 per cent, of the cases), brain abscess, and men- 
ingitis (in which it may be due to extension of the inflammation). The 
lesions are usually bilateral, and consist of congestion and swelling of the 
disk, blurring of its edges, and filling of the physiological cup. Often 
there is an associated neuroretinitis. The process may subside, but optic 
atrophy is the common sequel. The early stages of the disorder are to 
be recognized only by ophthalmoscopic examination, since considerable 
progress may be made before there is notable impairment of vision. 

Optic Atrophy. — Optic atrophy may occur secondarily to the causes 
that set up papillitis. Primarily it occurs as (1) a congenital, family 
disease (Leber's disease), most common in adolescent males, but usually 
transmitted by the females; and (2) in tabes dorsalis, paretic dementia, 
and sometimes in other nervous disorders. The lesions consist of 
gradually increasing pallor of the disk, with a well-defined edge, which 
in the secondary form may be irregular in outline; the artery may ap- 
pear normal or become small. The symptom is gradual failure of vision. 

The Optic Chiasm. — The chiasm is most frequently disordered by 
tumors of the brain, especially of the pituitary body (akromegaly). The 
fibers that supply the inner half of each retina (temporal field of vision) 
are commonly first involved, so that the symptom is double temporal 
hemianopia. Eventually, with progress of the disease, total blindness 
may ensue. Rarely two symmetrically situated tumors may implicate 
the fibers proceeding to the outer half of each retina (nasal field of 
vision) and bilateral nasal hemianopia may ensue. 



816 ' DISEASES OF THE NERVES 

The Optic Tract and Centre. — Disease of the optic tract between the 
chiasm and the cortex (cuneate portion of the occipital lobe) results in 
failure of vision of the temporal half of the retina of the corresponding 
side and of the nasal half of the retina of the other side (partial or com- 
plete homonymous hemianopia). The lesion may be in the fore part of 
the optic tract, in or about the thalamus, the lateral geniculate body, the 
corpora quadrigemina, the posterior part of the internal capsule, the optic 
radiation, or the cuneus. Disease of the supramarginal and angular 
gyrus may result in crossed amblyopia (concentric diminution of both 
fields of vision, usually more marked on the side opposite the lesion) and 
visual aphasia (word blindness, mind blindness). Resort to Wer- 
nicke's hemiopic pupillary reaction may enable one to determine whether 
the lesion is in advance of or posterior to the corpora quadrigemina: if 
throwing a bright light into the blind half of the retina results in con- 
traction of the pupil, it shows integrity of the reflex arc (the optic nerve 
fibers, the centre for the pupil, and the third nerve), and the lesion is there- 
fore in the optic radiation or the visual centre in the cuneus. Hemi- 
anopia usually means an organic lesion; rarely it may be found in 
hysterical disorders. Various sorts of aphasia may be associated with it. 

III. Oculomotor Nerve; IV. Trochlear Nerve; VI. Abducens 
Nerve. — The third nerve supplies the superior, internal and inferior 
recti, and the inferior oblique muscles of the eyeball, as well as the levator 
palpebral superioris, the ciliary muscle, and the constrictor of the iris. 
The fourth nerve supplies the superior oblique, and the sixth nerve the 
external rectus muscles. The dilator of the iris is innervated by the 
sympathetic. Paralysis of the third nerve results in ptosis, wrinkling of 
the forehead (to compensate for the lost power of the levator palpebral), 
divergent strabismus, diplopia, and a fixed and dilated pupil (cycloplegia) 
inactive to light and accommodation (iridoplegia). The eyeball is 
pulled outward by the active external rectus, and may be moved slightly 
downward and inward by the active superior oblique. Paralysis of the 
fourth nerve results in diplopia, especially when the patient looks down- 
ward, and perhaps deficient downward and inward movement of the 
eyeball (usually slight and unnoticed). Paralysis of the sixth nerve 
results in deficient movement of the eyeball outward or internal stra- 
bismus, and diplopia when the patient looks outward toward the affected 
side. 

The diplopia that results from paralysis of the ocular muscles 
may be homonymous (simple) when the false image (that seen by the 
affected eye) is on the same side as the paralyzed eye (usual in convergent 
strabismus) ; or the diplopia may be crossed, when the false image is seen 
on the other side of the true image (usual in divergent strabismus). In 
addition to restriction of movements of the eyeball, strabismus, and 
diplopia, paralysis of the ocular muscles usually leads to (a) secondary 
deviation of the sound eye, which may be demonstrated by covering the 
sound eye and directing the patient to fix on an object with the paralyzed 
eye toward the direction of paralysis; upon uncovering the sound eye, 



DISEASES OF THE CRANIAL NERVES 817 

it will be seen to have been moved farther in the direction of fixation than 
the paralyzed eye, on account of the greater response to an equal inner- 
vation on the part of the normal muscles of the non-paralyzed eye; and 
(b) erroneous projection of the field of vision. 

Occasionally, from overstimulation in hysterical states, in meningitis, 
etc., spasm of the ocular muscles may be observed. Nystagmus, a clonic, 
usually bilateral spasm of the ocular muscles, causing involuntary, 
rhythmic, oscillatory movements of the eyeballs, occurs in Friedreich's 
ataxia, multiple sclerosis, and other diseases of the nervous system, in 
nodding spasms of children, in miners, etc. 

Ophthalmoplegia. — Disease of the nuclei of the ocular nerves results in 
the condition called ophthalmoplegia (nuclear ocular palsy), which is 
discussed on page 851. 

V. Trigeminal Nerve.— The fifth nerve is made up of motor fibers 
which supply the muscles of mastication, and sensory fibers which, 
through the medium of its three great branches (ophthalmic, superior and 
inferior maxillary), supply hal^of the face and the anterior portion of the 
head, the conjunctiva, orbit, eyeball, nose, nasal cavity, lips, teeth, 
mouth, hard and soft palate, and anterior two-thirds of the tongue. Some 
observers also believe that the nerve conveys special taste fibers to the 
anterior two-thirds of the tongue. Paralysis of the motor portion of the 
nerve gives rise to loss of power of mastication on the affected side, in- 
ability to move the jaw toward the sound side (pterygoid muscle), and 
deviation of the jaw, when depressed, toward the paralyzed side. Irri- 
tation of this motor portion gives rise to spasm of the muscles of masti- 
cation (trismus), which may be tonic (as in tetanus, tetany, hysteria, 
reflex local irritation) or clonic (as in "chattering teeth," chorea, etc.). 
Disease of the sensory portion of the nerve (including the Gasserian 
ganglion) may give rise to : (1) Neuralgia, which usually involves one of 
the three great divisions, sometimes all three, and is often intractable 
(tic douloureux); (2) neuritis and herpes zoster; (3) anesthesia of part 
or all the area of distribution; and (4) nutritional or trophic disorders, 
such as lessening of the lacrymal secretions (to which conjunctivitis and 
ulceration of the cornea may be due) and of the salivary and buccal 
secretions, facial hemiatrophy, etc. Some observers believe that loss of 
the sense of taste over the anterior two-thirds of the tongue follows disease 
of the fifth nerve, but the available evidence is not conclusive. 

VII. Facial Nerve. — The facial nerve innervates the muscles of the 
face; perhaps it contains also some sensory fibers (geniculate ganglion 
and nerve of Wrisberg — Hunt). Paralysis of the nerve may be central 
or peripheral. 

Central Facial Paralysis. — The central case may be due to disease of (1) 
the nuclei in the pons ; this occurs in tumors, hemorrhage, and softening, 
and is usually associated with disease of adjacent nuclei; or (2) the 
fibers above the nuclei in the pons, the peduncle, the corona radiata, 
the internal capsule, or the cortex. This is usually a part of hemiplegia, 
and is due to like cause — hemorrhage, softening, tumors, abscess, etc.; 
52 



818 DISEASES OF THE NERVES 

rarely the facial nerve may be involved alone (internal capsule or cor- 
tical disease). This central paralysis differs from the peripheral type 
in the common freedom of the upper branches of the nerve (so that the 
patient can wrinkle the forehead and elevate the eyebrow) ; in the preser- 
vation of the normal electrical reactions of the nerve and muscles; and 
in the much less impairment of the emotional movements (laughing, 
crying) as contrasted with the voluntary movements of the facial 
muscles. 

Peripheral Facial Paralysis (Bell's Palsy). — Peripheral facial paralysis 
may result from (1) disease of the pons, usually tumors, softening, or 
inflammatory processes ; or the paralysis may be part of a hemiplegia, in 
which event it comprises a so-called crossed paralysis — involvement of 
the face on the side of the lesion (the facial fibers have already decus- 
sated) and involvement of the arm and leg on the opposite side; (2) 
disease at the cerebellopontine angle, at the base of the brain where 
the nerve emerges from the pons — usually tumors, gummas, tubercles, 
meningitis, traumas; (3) disease in the Fallopian canal — caries and 
inflammation, especially the results of middle-ear suppuration; (4) dis- 
ease outside the stylomastoid foramen — traumas, tumors of the parotid 
region, the influence of cold. The cases to which the term Bell's palsy 
is restricted are commonly attributed to cold and exposure (doubtless 
some infection). The lesions are inflammatory in nature and are usually 
most marked within the Fallopian canal, the unyielding wall of which 
leads to compression and atrophy of the nerve fibers. The symptoms 
(since the disease is a disorder of the lower motor neuron) consist of 
paralysis of muscles innervated by the nerve, together with wasting and 
fibrillary twitchings of the muscles and the electrical reactions of degen- 
eration. The face becomes flattened, the nasal fold obliterated, the angle 
of the mouth drooped (that of the other side looks and may become 
retracted), and there is inability to wrinkle the forehead, to frown, to close 
the eyelids, to show the teeth, etc. There may also be impairment of 
hearing (branch nerve to the stapedius), and of taste over the anterior 
two- thirds of the tongue (chorda tympani). The cutaneous sensibility 
is preserved. Complete recovery is unusual ; secondary contractures are 
common. The treatment comprises the use of hot applications, counter- 
irritation, massage, faradization, the iodides, etc. ; the treatment proper 
to any local disorder that may be present; and in cases not soon 
improved (three to four months) anastomosis of the spinal accessory 
or the hypoglossal with the facial nerve. 

Facial Spasm. — Facial spasm may be an organic disorder or it may 
arise reflexly from irritation due to carious teeth, for instance. The 
spasm may involve some or all the muscles supplied by the facial nerve, 
and may be unilateral or bilateral. Usually the muscles about the eye, 
or these and those of the side of the face, reveal rapidly recurring twitch- 
ings. The disorder is painless, although the nerve may have various 
tender spots. Occasionally, as after paralysis, tonic spasms of the facial 
muscles may ensue. Most of the cases of facial spasm last many years, 



DISEASES OF THE CRANIAL NERVES 819 

and are scarcely curable, although benefit may follow removal of sources 
of irritation, counterirritation, surgical intervention, etc. 

VIII. — Auditory Nerve. — The eighth nerve consists of two parts, the 
cochlear nerve, which connects the organ of Corti in the cochlea with the 
temporosphenoidal lobe and is the nerve of hearing; and the vestibular 
nerve, which connects the vestibule and the semicircular canals with 
cerebellar and other centres and serves to maintain equilibrium. 

Cochlear Nerve. — Disorder of the cochlear nerve gives rise to tinnitus 
aurium; sometimes to hyperacute or painful hearing (hyperacusis) ; 
most often to nervous deafness. If a tuning-fork is not well heard when 
held near the auditory meatus, but is well heard when placed on the 
temporal bone (the vibrations being transmitted through the bone to the 
cochlea and vestibule), the deafness is probably not nervous (not due to 
disorder of the nerve). 

Vestibular Nerve; Meniere's Disease. — Disorder of the vestibular nerve 
is the cause of so-called auditory vertigo, or Meniere's disease, a symptom 
complex, consisting of tinnitus aurium, vertigo, nausea, and vomiting, 
developing suddenly and sometimes attended by nervous deafness. The 
paroxysms occur irregularly — at long or short intervals. In addition, 
there may be nystagmus, diplopia, ataxia, etc. Rarely the disease is 
of the apoplectiform type, due to hemorrhage in the labyrinth; usuallv 
it occurs in those the subjects of acute or chronic ear disease — of the 
Eustachian tube, the middle ear, or the internal ear; it may be due to 
angioneurotic disturbances in the labyrinth; or attacks may be provoked 
by cerumen in the auditory canal, syringing the ear, etc. The prog- 
nosis in Meniere's disease is not good. Relief may be afforded by 
treating any local source of irritation, correcting refractive errors, the use 
of bromides, nitroglycerin in the event of arteriosclerosis and high blood 
pressure, etc. 

IX. — Glossopharyngeal Nerve. — The ninth nerve supplies motor 
fibers to the stylopharyngeus muscle and perhaps the palate, sensory fibers 
to the upper part of the pharynx, tonsil, soft palate, etc., and taste 
fibers to the posterior third of the tongue. The nerve scarcely, if ever, is 
diseased alone, being intimately related to the vagus. However, im- 
pairment of the sense of taste on the posterior third of the tongue and 
difficulty in swallowing may be attributed to it. 

X. Pneumogastric or Vagus Nerve.— The tenth nerve supplies the 
pharynx, larynx, lungs, heart, oesophagus, and stomach, and is intimately 
associated with the glossopharyngeal, spinal accessory, hypoglossal, and 
sympathetic nerves. Disease of the nuclei of these nerves constitutes 
bulbar paralysis. In paralysis of the pharyngeal branches of the vagus 
(together with the glossopharyngeal) there is difficulty in swallowing, 
food is not passed on to the oesophagus, and may regurgitate through the 
nostrils. Spasm of the pharyngeal muscles may be seen in hysterical 
subjects, and is the obtrusive feature of hydrophobia. Paralyses of the 
laryngeal branches of the vagus causes bilateral paralysis (nuclear dis- 
ease) or unilateral paralysis (usually nerve disease) of the laryngeal 



820 DISEASES OF THE NERVES 

muscles. Bilateral paralysis of the abductors (posterior crico-arytenoids) 
occurs in central disease (tabes, bulbar paralysis), pressure on the nerves, 
hysteria, etc., and is characterized by inspiratory stridor, more or less 
disordered phonation, and the cadaveric position of one or both vocal 
cords. Unilateral abductor paralysis follows involvement of one recur- 
rent laryngeal nerve — usually pressure due to an aneurysm of the aorta, 
and is characterized by hoarseness of the voice and a brassy cough. Ad- 
ductor paralysis is occasionally seen in hysteria; the vocal cords are not 
approximated during attempts at phonation, and the voice is lost. Spasm 
of the adductor muscles may occur in the event of central or peripheral 
irritation, and is a marked feature of laryngismus stridulus in rickety 
children. The cardiac branches of the vagus regulate and inhibit the 
action of the heart; irritation results in slowing of the heart beat, and 
paresis or paralysis (removal of inhibiting influence) results in accelera- 
tion of the beat. The subjective sensations of the heart beat are con- 
veyed to the brain by the vagus. Little is known regarding disorder of 
the pulmonary branches of the vagus, although these are said to influence 
the bronchial musculature and are perhaps in some way concerned in the 
paroxysms of bronchial asthma. Spasm of the oesophagus, of the cardia, 
and of the pylorus, vomiting, the gastric crises in tabes, and other gastro- 
intestinal disturbances are also related to disorder of the vagus. 

XI. Spinal Accessory Nerve. — The eleventh nerve, in part, joins 
the vagus nerve and is distributed with it; other fibers innervate the 
sternomastoid and the trapezius muscles. Paralysis of this part of the 
nerve results in paralysis of the sternomastoid muscle and inability to 
rotate the head to the opposite side, and of the trapezius muscle and 
lessened ability to elevate the shoulder, and the arm above the horizontal 
position. Complete paralysis of the trapezius does not ensue, since it is 
innervated in part by the cervical nerves. Spasm of the accessory nerve 
results in wryneck (torticollis). This may be a congenital (permanent) 
affection, due to shortening of the sternomastoid muscle (usually the 
right), and is often associated with facial asymmetry. An acquired 
spasmodic wryneck is common in women, especially hysterical subjects; 
it has been attributed to cold. The spasms may be tonic or clonic. 
When the sternomastoid is affected alone, the head is rotated to the oppo- 
site side, the chin somewhat tilted upward, and the occiput somewhat 
depressed; when the trapezius is also involved, the head is still further 
depressed toward the shoulder, and not so far rotated. The contracted 
muscles stand out as prominent tense cords. There is usually com- 
plaint of pain and stiffness of the neck. The cases that develop sud- 
denly after a cold usually recover promptly under the influence of hot 
applications, massage, and the salicylates internally. In the other cases 
the outlook is not so good and relapses are common. Relief may attend 
the use of the bromides, galvanism, mechanical fixation of the head, 
section of the contracted muscles, division of the accessory nerve, etc. 

XII. Hypoglossal Nerve. — The twelfth is the motor nerve of the 
tongue. The tongue is usually involved in hemiplegia (cortical or supra- 



DISEASES OF THE SPINAL NERVES 821 

nuclear lesion). Nuclear lesions occur in bulbar paralysis, tabes dorsalis, 
syringomyelia, tumors, etc., and unilateral disorder may follow tumors, 
meningitis, etc. The chief symptoms are unilateral or bilateral paralysis, 
atrophy, and fibrillary twitchings of the tongue; the mucous membrane 
of the tongue becomes wrinkled ; and difficulty is usually experienced in 
pronouncing certain words. Spasm of the tongue is unusual, but may 
be encountered in hysteria, epilepsy, chorea, stuttering, etc. 



DISEASES OF THE SPINAL NERVES. 

The Cervical Plexus. — Cervicooccipital neuralgia, involving the 
area of distribution of the first four cervical nerves (the occipitoparietal 
region), may be due to the causes of neuralgia mentioned elsewhere 
(page 808), or to local disease of the bone, the pressure of tumors, etc. 
The phrenic nerve, derived from the third, fourth, and fifth cervical 
roots (Fig. 16), may be paralyzed, in consequence of disease of the 
spinal cord (anterior horns), meninges, or vertebrae; of compression, 
as by a tumor; or of neuritis, etc. The symptoms consist of paralysis 
(immobility) of the diaphragm (unilateial or bilateral, as the case may 
be); immobility or retraction of the upper abdomen during inspiration, 
and, perhaps, bulging during expiration; and dyspnoea upon exertion. 
The inactivity of the diaphragm may be readily recognized by radio- 
graphic examination. The inaction due to inflammatory conditions, 
and the depression due to pleural effusion, emphysema, etc., must be 
excluded. Spasm of the diaphragm may be due to inflammatory or 
other irritative (sometimes so-called neurotic) conditions of the dia- 
phragm or phrenic nerve; and when intermittent, is shown by hiccough. 

The Brachial Plexus. — The brachial plexus is made up of the 
fifth, sixth, seventh, and eighth cervical and the first thoracic roots. 
Paralysis may be due to disease of the spinal meninges or the vertebrae; 
tumors and other compressing disorders of the neck; traumatism, such 
as fracture or dislocation of the vertebrae; stretching and laceration of 
the nerves; or neuritis. Since the root fibers combine variously to form 
the peripheral nerves, the clinical manifestations of a root lesion differ 
from those of a peripheral nerve lesion. The important clinical condi- 
tions comprise: (1) Obstetrical or birth paralysis (upper arm type of Erb), 
which results from laceration usually of the fifth and sixth, sometimes of 
all the roots, due to forcible stretching apart of the head and shoulder 
during birth. Usually the deltoid, biceps, supraspinatus, infraspinatus, 
brachialis anticus, and supinator longus are paralyzed and atrophied, 
but in some cases complete motor and sensory paralysis of the arm may 
occur (laceration of the entire plexus). (2) Lower arm type, due to 
involvement of the seventh and eighth cervical and the first thoracic roots. 
This is followed by paralysis of the triceps, pronators and flexors of the 
wrist, the flexors and extensors of the fingers, and the small muscles of 
the hand. Paralysis of the small muscles of the hand, anesthesia in 



822 



DISEASES OF THE NERVES 



the ulnar distribution, and ocular symptoms, due to disorder of the 
cervical sympathetic, together comprise Klumpke's paralysis. (3) Cer- 



Fig. 16 



A. to rectus lateralis 

to rectus antic, minor 
Anastomosis with hypoglossal 

Anastomosis withpneumogastric 
_2V. to rectus antic, major. 
N. to mastoid region . 

Great' auricular n. 

Transverse cervical n . 
N. to Trapezius, Ang. Scap. and Rhomboid. 

a clavicular n. 
Supra-acromial n . 
Phrcnie n . 

i\ r . to levator ang. scaj). 

N. to rhomboid 

Subscapular n. , 

Subclavicular n. 



N. to peetoralis major. 



Circumflex n. 

Musculo-cutaneous n. 
Median n. 
Radial n,„ 

Vlnar'n. 

Internal cutaneous n. 

Smullin.ternal cutaneous n. 




__Ezternal cutaneous i 
_. Qenito-crural n. 



Jf. to levator ani 
N. to obturator int. 

N. to ophincter ani. 
Coccygeal n. 



N..to gemellus infer. 
iV. to guadratus 
Small sciatic n . 
Sciatic n. 



The relations of the segments of the spinal cord and their nerve roots to the bodies and 
spines of the vertebrae. (Starr.) 



vical rib. An accessory cervical rib, usually compressing the seventh 
or eighth cervical roots or the subclavian artery, is a not uncommon 



DISEASES OF THE SPINAL NERVES 823 

cause of pain and paresthesia of the arm and hand, spasm and atrophy 
of the small muscles of the hand, local asphyxia, and even gangrene of 
the fingers. The condition may be familial, and may not become 
apparent until adult life. It is readily recognized upon radiographic 
examination, and is curable upon removing the accessory rib. 

Lesions of the individual nerves of the brachial plexus give rise to 
the following phenomena: (1) The circumflex nerve is often injured in 
dislocation of the shoulder and other injuries, etc., and leading to par- 
alysis and atrophy of the deltoid prevents raising the arm to the hori- 
zontal position. (2) The long or posterior thoracic nerve, which fixes 
and (with the trapezius) rotates the scapula, when paralyzed gives rise 
to a "winged" scapula, or prominence of the vertebral border (serratus 
paralysis), and imperfect elevation of the arm above the shoulder (less- 
ened rotation of the scapula). (3) The musculospiral nerve is often 
disordered — in consequence of cold, injuries, fracture of the humerus, 
etc.; of pressure, as by falling asleep with the arm on the back of 
a chair, counter, or bar (bartender's paralysis); or as may occur in 
so-called "bridal" paralysis and other paralyses resulting from a 
weight; and of lead poisoning and other forms of intoxication. Usu- 
ally the lesion is just above the elbow, and results in paralysis of the 
extensor muscles of the wrist and the fingers (except the supinator 
longus), and the characteristic wrist-drop. In lesions higher up, the 
triceps, the brachialis anticus, and the supinator longus are also involved. 
(4) The ulnar nerve, when paralyzed, results in atrophy and loss of 
power of the interossei, all the muscles of the little finger, the ulnar half 
of the deep flexors of the fingers, the adductor and the inner head of the 
short flexor of the thumb, and the ulnar flexor of the wrist. The con- 
spicuous symptoms consist of impaired flexion of the hand, loss of power 
of abducting and adducting the fingers, and of flexing and extending 
the second and third phalanges. There is also anesthesia of both sur- 
faces of the fourth and of the ulnar half of the third fingers. In long- 
standing cases the claw-like hand (main-en-grifTe) develops, being due 
to the activity of the non-opposed antagonistic muscles supplied by the 
median nerve. (5) The median nerve is rarely involved alone, but if 
so, it may lead to paralysis of the muscles arising from the inner condyle 
of the humerus (except the flexor carpi ulnaris) and the deep muscles 
of the forearm; in consequence, the arm cannot be pronated beyond the 
mid-position, the wrist cannot be flexed toward the radial side, the 
second phalanges cannot be flexed, and the thumb cannot be opposed 
to the ringer tips. There is also anesthesia of both surfaces of the 
thumb, and the first, second, and the radial half of the third finger. 
(6) Volkmann's contracture is a form of paralysis of the hand and fore- 
arm that usually follows fractures about the elbow or of the forearm 
and undue pressure caused by splints and tight bandaging. The nature 
of the disease is not definitely known; it has been attributed to defective 
blood supply (whence ischemic paralysis), to primary disorder of the 
muscles (myositis and fibroid changes), to neuritis, and to changes 



824 DISEASES OF THE NERVES 

following sloughing of the tissues of the forearm (which is sometimes 
observed). The symptoms consist of atrophy of the muscles of the 
forearm and hand, with contraction of the flexors, and the ultimate 
development of the claw-like hand. Usually there are no noteworthy 
sensory changes. The condition may be relieved by passive movements, 
massage, electricity, or operative measures. 

The Lumbar Plexus. — The lumbar plexus is made up of the first 
three lumbar roots and a branch from the fourth. The chief causes of 
disorder of the plexus are regional tumors, disease of the vertebrae, psoas 
abscess, and neuritis; and the obturator nerve may also be injured 
during parturition or by other trauma. The main symptoms consist 
of deficient adduction and rotation of the thigh (inability to cross the 
leg over the other). Paralysis of the anterior crural nerve results in 
paralysis and atrophy of the extensors of the knee, loss of the knee-jerk, 
and anesthesia of the anterolateral aspect of the thigh and of the inner 
aspect of the leg. Disease of the external cutaneous nerve may result 
in meralgia parcesthetica, a paresthesia of the outer aspect of the thigh. 

The Sacral Plexus.— The sacral plexus is made up of a branch 
from the fourth lumbar, the fifth lumbar, the first, second, and third 
sacral, and a branch from the fourth sacral roots. The chief causes of 
disorder of the plexus are pelvic growths and inflammations, disease of 
the vertebrae and the spinal meninges, parturition, and neuritis. In- 
volvement of the sciatic nerve causes sciatica (page 809). Paralysis of the 
nerve results in inability to flex the leg upon the thigh and loss of power 
of all the muscles below the knee; anesthesia of the outer aspect of the 
leg and of the sole and most of the dorsum of the foot; and ultimate 
wasting of the muscles. Paralysis of the external popliteal (or peroneal) 
nerve results in loss of power of the peroneal muscles, the extensors of 
the toes, and the tibialis anticus, with ensuing "foot-drop" and a char- 
acteristic, so-called, steppage gait. Paralysis of the internal popliteal 
nerve results in loss of plantar flexion of the foot and of the power to 
flex the toes, and anesthesia of the outer and posterior aspect of the 
lower leg and sole of the foot. 



DISEASES OF THE CERVICAL SYMPATHETIC NERVES. 

The cervical sympathetic system supplies vasomotor, secretory, and 
motor-nerve fibers to the head and neck and part of the arm and 
chest : vasomotor fibers to the bloodvessels, secretory fibers to the sweat 
glands and the submaxillary salivary glands, and motor fibers to the 
dilator muscle of the iris, the involuntary muscle fibers of the upper eye- 
lids, and the orbital muscle of Muller. The sympathetic nerves may be 
paralyzed or irritated, paralysis being much the more common. The 
symptoms of paralysis consist of unilateral ptosis, or narrowing of the 
palpebral fissure (paralysis of the unstriped muscle of the upper eyelid); 
enophthalmos or retraction of the eyeball (paralysis of Miiller's muscle) ; 






MENINGEAL HEMORRHAGE 825 

contraction of the pupil .and no dilatation when it is shaded (unopposed 
action of the sphincter muscle of the iris supplied by the intact third 
cranial nerve, which is also responsible for preservation of contraction of 
the pupil to light and in accommodation); unilateral pallor and lessened 
secretion of sweat (anidrosis); and perhaps dryness of one nostril and 
one-half of the mouth. Irritation of the sympathetic nerves causes 
contrary symptoms : widening of the palpebral fissure, protrusion of the 
eyeball (exophthalmos), dilatation of the pupil, flushing of the skin, and 
increased sweating (hyperidrosis). 



DISEASES OF THE CEREBROSPINAL MENINGES. 

MENINGEAL HEMORRHAGE. 

Etiology. — Meningeal hemorrhage may be extradural or intradura 
(subdural). Extradural cerebral hemorrhage is almost always trau- 
matic, though it may result from erosion of a vessel by caries of the bone. 
The middle meningeal artery is usually, but not always, the source of 
the hemorrhage. Intradural cerebral hemorrhage (hemorrhage from 
the vessels of the pia-arachnoid) may be due to traumatism (rather 
unusual), internal hemorrhagic pachymeningitis and associated disorders 
of mentality, rupture of an aneurysmal dilatation of a vessel, the hemor- 
rhagic diathesis, severe anemic states, paroxysms of whooping cough, 
the chronic congestion of cardiac, pulmonary, and advanced renal dis- 
eases; and it may occur from compression of the skull at birth. Spinal 
meningeal hemorrhage may or may not be associated with cerebral hemor- 
rhage; when it occurs it may be due to like causes; or it may result 
from local traumatism, and is then usually extradural. 

Symptoms. — The symptoms vary, depending upon the situation of 
the hemorrhage, upon whether it is small or excessive, and whether it 
occurs slowly or rapidly. In sudden, large, cerebral meningeal hemor- 
rhage the symptoms are much like those of intracerebral apoplexy, with 
the added evidences of cortical irritation or paralysis. In other cases 
the manifestations of the injury itself sometimes overshadow those of 
the hemorrhage, especially if the hemorrhage occurs slowly and is not 
directly over the motor area. In this event the patient may even con- 
tinue at his occupation for several hours, perhaps complaining only of 
headache; in other cases, there may be also some mental confusion, 
vertigo, and vomiting, and the patient gradually loses consciousness. 
Sometimes convulsions, which may be severe, occur; they may be uni- 
lateral and succeeded by paresis or paralysis (monoplegia or hemiplegia). 
In other cases, depending upon the seat of the hemorrhage, other symp- 
toms develop, such as aphasia, sensory disturbances, oculomotor palsy 
(occipital region), etc. In favorable cases the coma lessens and partial 
recovery of the palsy supervenes. 



826 DISEASES OF THE CEREBROSPINAL MENINGES 

The symptoms of spinal meningeal hemorrhage consist of pain and 
distress in the back, which are usually of sudden onset (in traumatic cases 
especially); radiation of the pain along the nerve roots and peripheral 
nerves, especially into the legs; and some muscular spasm. The deep 
reflexes may be temporarily lessened; usually they become exaggerated. 
In the event of compression of the cord, more or less paralysis super- 
venes and control of the vesical and rectal sphincters may be lost. 

Treatment. — The treatment of cerebral meningeal hemorrhage is simi- 
lar to that of intracerebral hemorrhage; but in every case the head 
should be shaved and searched for subcutaneous hemorrhage or frac- 
ture, and the question of operative removal of the clot must be consid- 
ered. When in doubt, it is probably wise to operate, since a large 
hemorrhage may result in death from compression, and a small hemor- 
rhage, if recovered from, may determine traumatic epilepsy or insanity 
in later life. In spinal meningeal hemorrhage resort should be had to 
lumbar puncture, with a view to relieve pressure; but if symptoms of 
compression of the cord ensue, laminectomy should be performed and 
the fluid and clotted blood removed; otherwise, the treatment consists 
of rest and quiet. 

EXTERNAL PACHYMENINGITIS. 

Etiology. — Inflammation of the outer surface of the dura mater is 
practically always a secondary affection, and is usually acute, although 
it may be chronic. It results from trauma (injuries to the skull or ver- 
tebrae) or bacterial infection — most commonly in consequence of necrosis 
of the petrous portion of the temporal bone in middle-ear disease, or of 
streptococcic or staphylococcic, less commonly of tuberculous or syph- 
ilitic, disease of the bones or adjacent tissues. The chronic cases are 
virtually always due to syphilis or tuberculosis. 

Pathology. — In acute cases the dura is swollen, softened, hemor- 
rhagic, and frequently suppurative. The pus collects between the 
membranes and the skull or vertebrae, and may extend into and between 
the two layers of the membrane (causing thrombosis of the sinuses), and 
involving the pia-arachnoid. In syphilitic and tuberculous cases the 
dura may be greatly thickened and considerable pus may be present, 
although the inner surface may be quite smooth. In chronic pachy- 
meningitis the lesions consist of the formation of the new fibrous tissue. 

Symptoms. — The symptoms in mild cases are indefinite; in the cerebral 
cases there may be only headache. In severe cases the symptoms of 
the primary disturbance often mask the pachymeningitis. Symptoms, 
when present, consist of headache, malaise, and perhaps convulsions, 
followed by drowsiness and stupor, and in case of suppuration, by 
chills and fever, and often sweats and leukocytosis. Sometimes the 
symptoms are only those of pressure, which may be sufficient to cause 
paralysis of the opposite side of the body. Choked disk has also been 
noted. Sinuses communicating with the exterior usually suggest 



INTERNAL PACHYMENINGITIS 827 

syphilis. The symptoms in the spinal cases are those of compression of 
the spinal cord, which are usually due, in part, also to associated lesions. 
. Treatment. — The treatment varies with the cause. In the lighter 
grades of the disease, antiphlogistic measures and counterirritants are 
indicated; in the severer grades, operative interference; and in syph- 
ilitic cases, mercury and potassium iodide. 

INTERNAL PACHYMENINGITIS. 

Three forms of internal pachymeningitis are usually described: The 
hemorrhagic, the purulent, and the pseudomembranous. The purulent 
and the pseudomembranous forms are uncommon and rarely recognized 
before death. The purulent form is usually secondary to inflammation of 
the pia-arachnoid, but it may follow softening of a sinus thrombus or 
result from traumatism. The pseudomembranous form is of obscure 
etiology, though it may result from trauma, or syphilis, or follow hemor- 
rhagic or suppurative pachymeningitis. The lesions may be purely 
fibrous or partly osseous. 

Internal hemorrhagic pachymeningitis may involve the cerebral 
or the spinal meninges. The lesions are most common in the brain 
(hematoma of the dura mater), and occur chiefly in males over fifty 
years of age, though they are by no means rare in children. The most 
frequent causes are: (1) Chronic alcoholism; (2) different nervous dis- 
turbances, such as paretic dementia, chronic hereditary chorea, senile 
dementia, etc. — whence it is frequently seen in insane asylums and 
almshouses; (3) cranial injuries; (4) different infectious diseases; (5) 
diseases of respiration, of circulation, and of nutrition. 

Pathology. — The lesions are usually confined to the area of distribu- 
tion of the middle meningeal artery and are often bilateral; they consist 
of the development of a very delicate vascular membrane (the result of 
the organization of an inflammatory exudate), the bloodvessels of which 
commonly rupture and give rise to the extravasation of a greater or less 
amount of blood (hematoma). Through the successive formation of 
such vascular membrane and the occurrence of hemorrhage, lamellae 
of membrane and hemorrhage are formed, which mav be 3 to 5 mm. 
thick. The lamellated structure is well shown on section, and frequently 
the successive layers may be stripped off. The brain is correspond- 
ingly compressed. Occasionally, in consequence of the imperfect organ- 
ization of the blood clot, a collection of serous fluid or a cyst results 
(hygroma dura matris). Involving the spinal meninges, the lesions are 
most common in the cervical region — hypertrophic cervical pachy- 
meningitis. A new formation, analogous to that in the brain, develops 
between the dura and the spinal cord, compressing the cord and the 
nerve roots, and often leading to secondary degenerations. 

Symptoms. — In many cases of the cerebral disorder symptoms are 
wanting, especially when the hemorrhage is small and has occurred 
slowly; and in the insane, in whom the insanity often masks the symp- 



828 DISEASES OF THE CEREBROSPINAL MENINGES 

toms of the pachymeningitis. Characteristic symptoms, however, consist 
of recurring apoplectiform attacks (referable to repeated hemorrhages), 
evidences of increasing intracranial pressure, and paresis or paralysis of 
cortical origin. Headache is common. The symptoms of increasing 
intracranial pressure consist of increasing headache, somnolence, pro- 
gressing in some cases to coma, nausea, vomiting, slowing and irregu- 
larity of the pulse, and contracted pupils (with marked or complete loss 
of reaction to light). Paralysis of one limb, or of a single cranial nerve 
(such as the facial or hypoglossal), and circumscribed or unilateral 
convulsions, suggest the cortical seat of the disorder. The patient often 
recovers from minor attacks, the manifestations of the apoplectiform 
insult gradually (within several weeks) subsiding, though paresis or 
paralysis, headache, intellectual disturbances, muscular weakness and 
awkwardness, etc., often persist. In severe cases the manifestations are 
often bilateral, and the patient may die in coma — an event that happens 
sooner or later in all cases, whether the lesions are unilateral or bilateral. 

The symptoms of the spi?ial disorder consist of severe neuralgic pains 
in the neck and arms (corresponding to the cervical roots involved), with 
associated hyperesthesia, paresthesia, and perhaps anesthesia. In the 
course of time muscular weakness and atrophy supervene; these depend 
upon the situation and extent of the nerve-root involvement, but are 
usually most marked in the small muscles and the flexors of the hands. 
The extensors often remaining intact, gradually lead to the development 
of the claw-like hand. In some cases the hands, forearms, upper arms, 
and shoulders may be markedly involved (cervical paraplegia). Ulti- 
mately spastic paraplegia may develop in the legs from secondary 
degeneration in the cord. 

Diagnosis. — The diagnosis of the cerebral disorder is always difficult; 
it is suggested by the etiological factors and recurring apoplectiform 
attacks, with evidences of cortical irritation. The spinal disorder must 
be differentiated from tumors and other forms of compression, amyo- 
trophic lateral sclerosis (absence of severe initial pains and sensory 
changes), and syringomyelia (characteristic sensory changes). 

Prognosis. — The outlook in both types of the disorder is bad. 

Treatment. — The causal condition demands first attention, and the 
symptoms should be treated as they arise: during the stage of hemor- 
rhage — rest in bed, elevation of the head, an ice-cap or leeches to the 
base of the head or behind the ears, hot foot baths, venesection, free 
purgation, etc. ; and during the subsequent stages — mercurials, potassium 
iodide, and antispasmodics. Should the diagnosis of a focus of cortical 
irritation be possible, especially with evidences of increasing intracranial 
pressure, an operation for the removal of the clot may be undertaken. 

LEPTOMENINGITIS. 

Etiology. — Inflammation of the pia-arachnoid (leptomeningitis, pia- 
arachnitis) may be primary or secondary, and acute or chronic. The 



LEPTOMENINGITIS 829 

primary acute form, even the sporadic cases, is commonly the cerebrospinal 
fever (meningococci infection) already discussed (page 86), although 
tuberculous and pneumococcic infections also may occasion lesions only, 
or most marked, in the meninges. Secondary leptomeningitis may be 
due to: (1) Bacterial infection, and is seen most commonly, as a com- 
plication or sequel, in the acute infectious diseases, especially in pneu- 
monia, septicemia, erysipelas, acute infective endocarditis, typhoid 
fever, smallpox, measles, scarlet fever, gonorrhoea, influenza, acute 
rheumatic fever, lung abscess, empyema, etc. It results also from 
extension of infection from caries of adjacent bones, from purulent otitis 
media, disease of the frontal sinuses, nasal cavities, or pharynx, brain 
abscess, etc. (2) Trauma of the bones of the skull, affecting the men- 
inges directly; but in most of these cases, trauma and infection are 
associated. (3) As a terminal infection in many chronic diseases, such 
as nephritis, diabetes, arteriosclerosis, etc. The exciting causes may be 
the microorganisms provocative of the primary infection, but often they 
are the common pyogenic bacteria, the infection of the meninges being 
hemogenic, lymphogenic, or occurring by contiguity of tissue. 

Pathology. — The lesions vary much in different cases. Basal menin- 
gitis, convexity meningitis, and ventricular meningitis are terms used 
to denote the seat of the marked lesions; but in many cases the lesions 
are more or less widespread. In the meningitis following pneumonia 
and sepsis the convexity on both sides is usually involved; in that 
occurring in children the posterior basic region is especially involved 
(posterior basic meningitis), and this is also true of that occurring in 
Bright's disease, diabetes, and other cachectic conditions. Anatomic- 
ally, three varieties may be distinguished — the serous meningitis of 
Quincke, tuberculous meningitis (page 122), and purulent meningitis. 

The serous meningitis of Quincke is a rare condition, in which the pia- 
arachnoid is the seat of serous inflammation, especially marked on the 
convexity, and in which, by lumbar puncture, the cerebrospinal fluid is 
found under greater pressure than the normal 40 to 60 mm. of w T ater, 
and it contains at least twice as much as the normal (0.5 per cent.) of 
albumin. 

Generally, however, the lesions are purulent and confined to, or at 
least most marked on, the convexity of the brain (convexity meningitis). 
In some cases, especially in infants or children, they are more marked at 
the base (posterior basic meningitis). In other cases the lesions are 
widespread, and consist of swelling, congestion, and suppuration of the 
pia-arachnoid, sometimes its more superficial layers, especially marked 
along the course of the vessels, and sometimes so marked as completely to 
obscure the convolutions. They are usually bilateral, although they may 
be unilateral, especially in cases due to extension from middle ear disease, 
etc., when they may be accompanied by sinus thrombosis. The ventricles 
may contain, and are sometimes distended with, serous or seropurulent 
fluid; the lesions may extend to, or simultaneously involve, the spinal 
meninges (cerebrospinal meningitis); and in some cases small foci of 



830 DISEASES OF THE CEREBROSPINAL MENINGES 

hemorrhage may be detected in the superficial layers of the brain 
(meningo-encephalitis). 

Chronic leptomeningitis is quite uncommon; it may be due to syphilis 
or tuberculosis; rarely the meningococcic (epidemic or sporadic) cases, 
posterior basic meningitis, and the serous meningitis of Quincke may 
run a chronic course. 

Symptoms. — The symptoms are sometimes divided into the pro- 
dromal, the irritative, and the paralytic. Prodromal symptoms are 
frequently absent, but sometimes for a day or two there may be general 
malaise, irritability, headache, and perhaps vomiting; but these are 
often overshadowed or masked by the evidences of the primary disorder. 
The disease is often ushered in with high fever, perhaps a chill or chilli- 
ness, and headache which is extreme, persistent, sometimes more marked 
in the frontal region, but usually widespread — constituting a most char- 
acteristic symptom of the disease. With the progress of the inflamma- 
tion, the headache increases in severity, and is often subject to exacer- 
bations of great severity (occasioning the so-called "hydrocephalic 
cry"), and disorders of consciousness — delirium, stupor, coma — super- 
vene. Furthermore, manifestations of cerebral irritation develop, and 
vary somewhat with the seat of the most marked lesions; they com- 
prise vomiting (often frequent and persistent, especially in basilar menin- 
gitis); slowing and irregularity of the pulse; retraction of the head and 
rigidity of the neck muscles (opisthotonos), especially when the lesions 
are posterior, and basal, and cervical; crunching of the teeth; pupillary 
miosis; strabismus; nystagmus; photophobia; undue sensitiveness of the 
auditory apparatus; ptosis; muscular irritability and twitchings; con- 
vulsive seizures in the facial muscles (trismus) and in the extremities; 
increase of the reflexes; Kernig's sign (inability to extend the leg when 
the thigh is flexed on the abdomen); general cutaneous and muscular 
hyperesthesia; etc. These are soon followed by evidences of paresis 
or paralysis (paralytic stage): coma instead of the previous delirium 
and stupor; increased frequency of the pulse (not constant); pupillary 
differences or mydriasis; sometimes optic neuritis (basilar meningitis); 
paralysis of certain cranial nerves (especially the facial) or paresis of the 
extremities of cortical nature; loss of reflexes; retraction of the abdomen; 
loss of control over the sphincters; etc. Fever is present throughout the 
course of the disease; it is usually irregular, varying up to 102° or 103° F., 
but occasionally hyperpyrexia is observed, and sometimes but little fever 
(in terminal infections). Repeated chills are not uncommon. Herpes 
labialis is quite common, but especially in the meningococcic infections. 
The urine is diminished and often contains albumin and casts; the 
bowels are constipated, until the final stage, when incontinence often 
supervenes. Leukocytosis is usually present. 

Diagnosis.— The diagnosis is usually comparatively easy, but in doubt- 
ful cases the antecedent history, disordered cerebration, high fever, slow 
pulse, and the other symptoms narrated, together with the data men- 
tioned on page 89, should clear up the diagnostic uncertainty. 



CEREBROSPINAL LOCALIZATION 831 

Prognosis.— The outlook depends upon the nature of the infection, 
the severity of the lesions, and the associated conditions. Quincke's 
serous meningitis may eventuate in recovery; the purulent cases are 
almost always fatal; and the non-fatal cases may be followed by divers 
sequels (page 89). 

Treatment. — The treatment is that mentioned on page 89. Perhaps 
in the future we may secure a serum or bacterin for each specific type of 
meningitis. 



DISEASES OF THE BEAIN AND SPINAL COED. 

CEREBROSPINAL LOCALIZATION. 

Diseases of the brain and the spinal cord may be somewhat arbitrarily 
divided into two classes: (1) The so-called system diseases — those in 
which the lesions are more or less strictly limited to certain tracts or 
collections of neurons functionally homologous; if only one tract is 
involved, the disorder is spoken of as a single system disease; if more 
than one, as a combined system disease. (2) The non-system (focal or 
diffuse) diseases — those in which the lesions are not limited to a system 
or systems of neurons. The system diseases involve variously the dif- 
ferent motor and sensory neurons, of which mention is made on page 
802 and thereafter, and which are shown in their course in the spinal 
cord on Plate II. (page 805). 

The accurate localization of irritative or destructive, system or non- 
system, disorders of the brain and spinal cord depends upon a knowl- 
edge of the functional activity and the mutual relations of the different 
parts of the brain and the cord. The characteristic features of disease 
of the upper and the lower motor neuron and of the sensory neuron 
are mentioned on pages 802, 803, and 804. When diseased focally, 
that is, when the seat of non-system diseases, most parts of the brain 
and cord exhibit sensible evidence of the local lesions that permit of 
definite localization; but there are certain so-called silent areas in the 
brain, the functions of which are unknown, and disease (especially 
tumors) of which, although causing general manifestations, provoke 
no localizing symptoms. In the diagnosis of local lesions, especially 
tumors of the brain, one must remember: (1) That focal signs are 
of the greater value the nearer to the general symptoms in point of 
time they develop ; (2) that some of the signs are often due to irritation 
or paralysis of adjacent areas of the brain or of tracts that may pass 
through or near the seat of disease, and that this is more likely to be 
the case the longer after the onset of the general symptoms these local- 
izing signs develop; and (3) that in advanced cases many of the signs are 
often due, not so much to the primary lesion (tumor, abscess, etc.) as to 
secondary conditions, such as meningitis, hydrocephalus, secondary 
tumors or abscesses, hemorrhage into tumors, and so forth. 



832 



DISEASES OF THE BRAIN AND SPINAL CORD 



The Brain. — Frontal Lobes; Prefrontal Region. — The frontal 
lobes anterior to and above the ascending and the third frontal convo- 



Fig. 17 




CONCRETE CONCEPT 

The lateral surface of the human brain, showing the localization of the different functions. (Mills.) 

Fig. 18 




The mesial surface of the human brain, showing the localization of the different functions. (Mills). 

lutions are believed to subserve the higher mental and psychic func- 
tions, such as general intelligence, memory, reasoning powers, judgment, 



CEREBROSPINAL LOCALIZATION 



833 



attention, volition, and abstract concepts (Figs. 17 and 18). Mills and 
other observers assign these functions especially to the left side in right- 
handed persons, and to the right side in left-handed persons. Tumors 
and other destructive lesions of the prefrontal region are said by Mills to 
be always associated with disorder of these higher mental functions. 

Motor Cortex; Ascending Frontal Convolutions. — The cor- 
tical centres for voluntary muscular movements are situated in the 
ascending frontal, second frontal, and paracentral lobules, the different 
centres being as represented in Fig. 19. A tumor or other lesion of the 
motor cortex, or immediately subjacent thereto (subcortical), may pro- 
duce, first, irritation of the area involved and spasm or convulsions of the 
muscles of the opposite side of the body therein represented (focal or 
Jacksonian epilepsy). Soon localized paresis or paralysis supervenes, 



Fig. 19 




The functional areas of the cerebral cortex of the left hemisphere, to show especially the cortical 
centres for voluntary muscular movements. (Starr.) 



and if at first limited to certain groups of muscles, may, as the tumor 
grows, become monoplegic or hemiplegic; it usually becomes spastic 
in type (degeneration of the upper motor neuron). In addition, there 
is likely to be disorder of epicritic sensibility, especially lessening of 
tactile sensibility and of the power of cutaneous localization. This is 
usually due to pressure or secondary involvement of the ascending 
parietal convolution where sensibility has its cortical representation. 
Homologous muscles that act together are not likely to show marked 
or permanent disability from unilateral cortical or subcortical lesions, 
since the muscles of both sides may be innervated from the one cerebral 
hemisphere. 

Sensory Cortex; Parietal Lobe. — The cortical centres for sen- 
sation are situated in the parietal lobe, especially in the ascending 
53 



834 DISEASES OF THE BRAIN AND SPINAL CORD 

parietal convolution and the gyrus fornicatus. According to Mills, 
these centres correspond with, and are about on a level with, the related 
motor centres in the neighboring frontal convolutions. Tumors and 
other destructive lesions of the parietal lobe causes disturbances of 
epicritic, protopathic, and deep (or muscular) sensibility — that is, dis- 
order of the sensations of touch, pain, temperature, and stereognosis. 
Usually also there are motor disturbances from compression by or exten- 
sion of the tumor to the frontal convolutions, or subcortical implication 
of the motor fibers in the corona radiata. 

Occipital Lobe. — Irritative lesions of the occipital lobe may cause 
convulsions with visual warnings. Destructive lesions involving the 
cuneate lobule cause simple or homonymous hemianopsia; those involving 
the angular gyrus cause bilateral contraction of the field of vision, 
greater on the side opposite the tumor, and visual aphasia (word-blind- 
ness), especially if situated on the left side. 

Temporosphenoidal Lobe. — Irritative lesions of the temporosphe- 
noidal lobe may cause convulsions with auditory warnings or auditory 
hallucinations. Destructive lesions cause deafness on the opposite side, 
and sensory aphasia (word-deafness), especially if situated on the left 
side. Lesions of the uncinate gyrus may cause olfactory and gustatory 
hallucinations. 

Centrum Ovale. — Lesions of the centrum ovale may involve the 
motor, sensory, or association fibers that pass through it. Subcortical 
'lesions cause motor or sensory disturbances similar to those mentioned 
in connection with the motor and the sensory cortex, but varying with 
the situation of the lesion (the fibers implicated). Convulsions do not 
occur unless the motor cortex is involved; if they do supervene, it is 
not until the paralysis has been present for some time (the reverse of 
cortical lesions). Lesions of the centrum ovale lower down resemble 
those of the internal capsule. 

Internal Capsule. — In the comparatively constricted region of the 
internal capsule practically all of the motor and sensory projection 
fibers of the cerebral cortex are closely packed together. The internal 
capsule is made up of a so-called knee; an anterior, lenticulo-caudate 
(lenticulo-striate) limb; and a posterior limb, of which the anterior 
two-thirds is called the lenticulo-optic (lenticulo-thalamic) segment, and 
the posterior one-third the retrolenticular segment. The different sets 
of neurons passing through the internal capsule are shown in Fig. 20. A 
lesion of the anterior segment, if not large, may cause only disorders of 
the higher mental and psychic faculties. A lesion of the knee gives rise 
to disturbances of the motor nerves of the eye, the motor part of the 
trigeminus, the facial, and the hypoglossal; in consequence, in addition 
to the obvious paralyses, disorders of articulation ensue, and if the lesion 
be on the left side, aphasia. A lesion just posterior to the knee (the 
pyramidal tract), implicating in order the neurons for the face, arm, and 
leg, causes usually hemiplegia of the opposite half of the body; mono- 
plegia is very rare, the lesion scarcely ever being small enough to involve 



CEREBROSPINAL LOCALIZATION 
Fig. 20 



835 



lizcicdis. 
JCnie. 

Hypocjlossus. 

_ Aim 
Coptic 

JBeuv 




rue. 

•Auditory 
tract. 



A horizontal section through the right hemisphere to show especially the internal capsule, the 
situation of common lesions therein, and their consequences: B. Kn., knee of the corpus callosum; 
Vh., anterior horn of the lateral ventricle; F s , inferior part of the third frontal convolution; 
l.stric, lenticulo-striate division of the internal capsule; Knie.ic, knee of the internal capsule; 
I. optic, lenticulo-optic division of the internal capsule; Th., optic thalamus; J., island of Reil; 
cl., claustrum; Operc., operculum; T x , first temporal convolution; r. lie, retrolenticular region of 
the internal capsule; C. A., amnion's horn; calc, calcarine fissure; Hh., posterior horn of the 
lateral ventricle; SS, optic radiation of Gratiolet; T 2 , second temporal convolution; Facialis, 
position in the capsule of the motor tract to the face; Hypoglossus, position of the tract to the 
tongue; Arm, position of the tract to the arm; Bein, position of the tract to the leg; S. B., 
sensory fibers; S., visual tract; Auditory tract, auditory tract. (After von Monakow.) 



836 DISEASES OF THE BRAIN AND SPINAL CORD 

only the neurons innervating one limb. A lesion of the posterior third 
(the retrolenticular segment) of the posterior limb of the internal capsule 
(which transmits sensory fibers for the entire body, as well as the optic 
and auditory neurons) gives rise to hemianesthesia (and related sensory 
changes) of the opposite half of the body, homonymous hemianopsia, 
and deafness on the opposite side. In most cases, however, notably in 
cerebral hemorrhage (of which the internal capsule is the common seat), 
the results are usually varying combinations of those mentioned. 

Thalamus. — Lesions of the thalamus usually implicate also the internal 
capsule, so that the symptoms are likely to be chiefly those just mentioned. 
In addition, there may be also loss of control of the facial expression 
and of emotional movements, and perhaps also imperfect control of the 
posture of the body, athetoid movements of the extremities, etc. 

Corpora Quadrigemina. — Lesions (usually a tumor) of the anterior 
bodies of the corpora quadrigemina cause oculomotor paralysis (pressure 
on the nuclei or subcortical interruption of impulses), dilated pupils 
inactive to light and accommodation, and, perhaps, nystagmus. Lesions 
of the posterior bodies give rise to auditory disturbances, deafness, 
difficulty in maintaining equilibrium, and a tendency to fall, usually to 
the opposite side. 

Crus; Cerebral Peduncle. — A lesion of one peduncle, as of the 
internal capsule, causes hemiplegia (face, arm, and leg) and hemianes- 
thesia on the opposite side of the body; paralysis of the ocular motor 
nerve of the same side (involvement of the nucleus or fibers); perhaps, 
also, if the lesion (tumor) is large, paralysis of the fourth, fifth, and sixth 
nerves. 

Pons. — A lesion in the pons causes contralateral hemiplegia and 
hemianesthesia, and usually paralysis of the face (facial nuclei) of the 
same side (crossed paralysis). In some cases there is also homolateral 
paralysis of the third, the fourth, the motor division of the fifth, and the 
sixth nerves; contralateral hemianesthesia (arm and leg) and homo- 
lateral anesthesia in the area of distribution of the sensory division of the 
fifth nerve (crossed hemianesthesia); or homolateral deafness (involve- 
ment of the eighth nerve). The lesion (tumor) if situated and growing 
near the median line of the pons, may cause motor paralysis (sometimes 
sensory paralysis) of one side; and paralysis of both facial (rarely other 
cranial) nerves. 

Medulla. — A lesion in the medulla may involve one or both pyram- 
idal tracts (which here are close together), and cause, therefore, unilateral 
or bilateral paralysis (usually more marked on one side than the other); 
and also paralysis of any or all of the cranial nerves from the eighth to 
the twelfth (bulbar paralysis, page 850). There may be also disturb- 
ances of respiration, disorders of the rate and rhythm of the heart, 
and glycosuria or polyuria. 

Pituitaey Body. — Tumors of the pituitary body (akromegaly, page 
356 ) usually compress the optic chiasm and cause at first double temporal 
hemianopsia (involvement of the fibers that supply the inner half of each 






CEREBROSPINAL LOCALIZATION 837 



retina, the temporal field of vision). Eventually, with growth of the 
tumor and involvement of the temporal portions of the optic chiasm 
and nerves (nasal field of vision), more or less complete blindness 
ensues. 

Cerebellopontine Angle. — Tumors of the cerebellopontine angle 
cause homolateral disturbances of hearing and of equilibration from 
involvement of the auditory nerve, which with the tumor seems usually to 
be intimately related; homolateral paresis or paralysis of the fifth, sixth, 
and seventh cranial nerves (from compression) ; controlateral hemiplegia 
and hemianesthesia from compression of the motor and sensory tracts 
in the pons; and evidences of disturbance of the cerebellum of the same 
side. 

Cerebellum. — Lesions (tumors) of the cerebellum give rise to homo- 
lateral motor weakness and hypotonia of the arm, leg, neck, and trunk; 
sometimes contralateral hemiplegia (from pressure on the pons and 
medulla); incoordination, usually more marked on the side of the lesion; 
inability to maintain equilibrium, an unsteady gait, and a tendency to 
turn and fall, usually toward the side of the tumor; and nystagmus. Any 
of the regional cranial nerves may be affected by compression. Vertigo 
is often very marked, and suggests Meniere's disease. Muscular 
rigidity, especially of the muscles of the neck, back, and trunk (opisthot- 
onos) may occur, and may be associated with muscular twitchings or 
tonic spasms, especially in disease of the middle lobe; in this event, the 
tendency may be to fall backward. 

Spinal Cord. — The localization of focal lesions of the spinal cord pre- 
supposes a knowledge of the functions of the segments of the cord, of 
the segmental muscular and sensory innervations, and of the reflex 
arcs represented in each segment. These are shown in Plate I, page 
803, and in the accompanying tables, I, II, and III, arranged by M. A. 
Starr (pages 838 and 839). 

Total Transverse Lesions. — A total transverse lesion, one in 
which that part of the cord below the segmental level of the lesion is 
entirely removed from all influences emanating from above, gives rise 
to: (1) Complete flaccid paralysis of all the muscles innervated by the 
cord below the segmental level of the lesion (this is in contrast to sub- 
total transverse lesions in which spastic paralysis occurs); (2) complete 
anesthesia below the segmental level of the lesion; (3) absent knee- 
jerks, and other deep reflexes below the segmental level of the lesion (occa- 
sionally certain of the cutaneous reflexes, such as the plantar reflex — dorsal 
flexion of the toe, the Babinski sign — may be preserved) ; (4) atrophy of 
the paralyzed muscles; (5) partial or complete reactions of degeneration; 
and (6) loss of control over the vesical and rectal sphincters. 

Subtotal Transverse Lesions. — Subtotal transverse lesions give 
rise to motor paralyses varying with the segmental level (Table I, page 
838), segmental sensory changes shown in Plate I, page 803, and 
disturbances of reflexes shown in Table II, page 839. In general, the 
important symptoms are those of myelitis (page 880). 



838 



DISEASES OF THE BRAIN AND SPINAL COHD 



Unilateral Lesions (Brown-Sequard Paralysis). — Lesions lim- 
ited to one lateral half of the spinal cord are occasionally seen in stab 
wounds, bullet wounds, syphilis, and tumors, and are rarely observed 
also in syringomyelia and spinal hemorrhage. They give rise to 
the following characteristic symptom-complex, named after Brown- 

Table I. — Showing the Muscles Represented in Groups of Cells in the Various 
Segments of the Spinal Cord. 



II., III. 


IV. 


V. 


VI. 


VII. 


VIII. 


I. 


Cervical. 


Cervical. 


Cervical. 


Cervical. 


Cervical. 


Cervical. 


Dorsal. 


Diaphragm. 


Diaphragm. 












Sterno- 


Lev.ang.scap. 












mastoid. 


Ehomboid. 


Rhomboid. 










Trapezius. 


Supra- and 


Supra- and 










Scalenus. . 


infraspin. 
Deltoid. 
Supin. long. 
Biceps. 


infraspin. 
Deltoid. 
Supin. long. 
Biceps. 
Supin. brev. 
Serratus mag. 


Biceps. 












Serratus mag. 












Pect. (clav.). 


Pect. (clav.). 












Teres minor. 


Pronators. 


Pronators. 










Triceps. 


Triceps. 












Brach. ant. 


Brach. ant. 












Long exten- 


Long exten- 












sors of wrist. 


sors of wrist 

and fingers. 
Pect. (costal). 
Latis. dorsi. 
Teres major. 
Long flexors 

of wrist and 

fingers. 


Long flexors 

of wrist and 

fingers. 
Extensor of 

thumb. 
Intrinsic 

muscles of 


Extensor of 

thumb. 
Intrinsic 

muscles of 












hands. 


hands. 



I. Lumbar. 


II. Lumbar. 


III. Lumbar. 


IV. Lumbar. 


V. Lumbar. 


Quadr. lumb. 










Obliqui. 










Transversalis. 










Psoas. 


Psoas. 








Iliacus. 


Iliacus. 
Sartorius. 
Quad. ext. cruris. 


Quad. ext. cruris. 

Obturator. 

Adductores. 


Obturator. 

Adductores. 

Glutei. 


Glutei. 

Biceps femoris. 

Semi-tend. 

Popliteus. 



I. Sacral. 



II. Sacral. 



Biceps feuior. 
Bemi-memb. 

Ext long. dig. 

Cast roc. 
Tibialis post 



Gastroc. 

Tibialis post. 

Tibialis anticus. 

Peronei. 

Intrinsic muscles of foot. 



III. Sacral. 



IV. and V. Sacral. 



Peronei. 

Intrinsic muscles of foot. 



Sphincter ani et vesicae. 
Perineal muscles. 



CEREBROSPINAL LOCALIZATION 



839 



Sequard: (1) On the side of the lesion: (a) motor paralysis on a level 
with and below the lesion — flaccid paralysis and atrophy, with the re- 
actions of degeneration, of the muscles innervated by the segment of 
cord destroyed, and spastic paralysis of the muscles innervated by lower 
motor neurons below the destroyed segment of the cord (due to degen- 
eration of the pyramidal tract — upper motor neuron); (b) a segmental 
zone of complete anesthesia (protopathic, epicritic, and deep sensi- 
bility) corresponding to the spinal-cord segment destroyed; and (c) below 



Fifth cervical to first dorsal. 

Fifth and sixth cervical. 
Sixth cervical. 
Seventh cervical. 

Sixth to eighth cervical. 



Table II. — Localization of Muscular Reflex Acts in the Spinal Cord. 

Reflex acts. Localization in segment. 

Pupillary reflex through the sympathetic : Dil- Fourth cervical to first dorsal. 

atation of the pupil produced by irritation of 

the neck. 
Scapular reflex : Irritation of the skin over the 

scapula produces contraction of the scapular 

muscles. 
Biceps and supinator longus : Tapping their 

tendons produces flexion of the forearm. 
Triceps reflex : Tapping tendon produces ex- 
tension of forearm. 
Scapulohumeral reflex : Tapping the inner lower 

edge of the scapula causes adduction of the 

arm. 
Tapping extensor tendons at the wrist causes ex- 
tension of the hand. 
Tapping flexor tendons at the wrist causes flexion Seventh to eighth cervical. 

of the hand. 
Palmar reflex : Stroking palm causes closure of Eighth cervical to first dorsal. 

fingers ; finger clonus. 
Abdominal reflex : Stroking side of abdomen Ninth to twelfth dorsal. 

causes retraction. 
Genital reflex : Squeezing the testicle causes 

contraction of the abdominal muscles. 
Patella tendon : Striking tendon at knee causes 

extension of the leg ; " knee-jerk." 
Achilles tendon reflex : Tapping the Achilles 

tendon causes flexion of ankle. 
Foot clonus : Extension of Achilles tendon 

causes flexion of the ankle. 
Plantar reflex : Tickling sole of foot causes First to third sacral. 

flexion of the toes. 
Babinski' s reflex : Scratching sole of foot causes 

extension of great toe and flexion of the 

others. 
Mendel's reflex : Tapping the tendons of the 

toes causes flexion or extension of the toes. 



First to third lumbar. 
Second and third lumbar. 
First to third sacral. 
First to third sacral. 



Table ILL — Localization of Skin Reflexes in the Spinal Cord. 

Keflex acts. Localization in segment 

Epigastric reflex : Stroking breast causes dim- Seventh to ninth dorsal. 

pling of the epigastrium. 
Cremasteric reflex : Stroking inner side of thigh First and second lumbar. 

causes retraction of scrotum. 
Gluteal reflex : Stroking buttock causes dim- Fourth to fifth lumbar. 

pling in the fold. 



840 



DISEASES OF THE BRAIN AND SPINAL CORD 



the level of the lesion — normal or increased protopathic and epieritic 
sensibility, but usually lessening of the deep sensibility (muscle sense). 
(2) On the side opposite the lesion: (a) lessened protopathic (pain) 
and epieritic (tactile and temperature) sensibility; and (b) normal deep 
sensibility, muscular power, and reflexes. 



APHASIA. 



The following statements are largely adapted from Starr's discussion 
of aphasia : 

The basis of language is a series of memory pictures of: (1) The sound 
of a word; (2) the effort necessary to enunciate it; (3) the appearance 
that its printed or written symbols present; and (4) the effort needed to 



Fig. 21 



Hand 



Touch 




Voice 



Hearing 



Diagram to illustrate aphasia. The cortical, sensory, and motor centres are indicated by the 
arrows. The secondary cortical centres of memories are indicated by circles. /, visual, of objects; 
//, visual, of words; ///, tactile; IV, auditory; V, speech; VI, writing. These are joined to one 
another by association fibers which transmit impulses in both directions. Subcortical lesions in 
these fibers as well as lesions in the cortex, cause aphasia. (Starr.) 

produce these symbols in writing. These memory pictures are inti- 
mately connected with one another by means of association fibers 
which pass in nil directions between the areas in which they are located, 
:iik1 they are also joined to the memory pictures which make up the con 
cept (Fig. 21). They are so intimately joined that if one is lost all tin 



the 



APHASIA 841 

otheis feel the effect, and a break in the mechanism leads to a defect 
in the act of speech. The loss of speech or of the power of compre- 
hending the spoken or written language is termed aphasia; the loss of 
concepts (inability to understand the uses of familiar objects) is termed 
apraxia. 

Etiology. — Aphasia is occasionally said to be functional in nature, 
being due to a temporary disturbance of the speech centres, such as may 
occur in epilepsy, hysteria, intoxications like alcoholism, uremia, etc., 
and angiospasm of the cerebral bloodvessels (in which condition there 
is usually also some anatomical disorder of the vessels). In the great 
majority of cases, however, aphasia is due to a destructive anatomical 
lesion, such as cerebral hemorrhage, softening (embolism or throm- 
bosis,) abscess, or tumor; and the lesion may involve the centres (cortical 
aphasia) or the tracts (subcortical aphasia). 

Types of Aphasia. — Aphasia is broadly divided into sensory and motor. 
Sensory aphasia consists in a lack of power to recognize or to recall the 
sound or appearance of words. If the sound alone is lost, the condition 
is termed word-deafness; if the appearance is lost, the condition is 
termed word-blindness. Motor aphasia consists in a lack of power to 
initiate the effort and set in action the motor mechanism needed to pro- 
nounce or to write a word. The former is termed motor or ataxic 
aphasia, the latter motor agraphia; they are usually combined. 

Word-deafness. — If the memory of the sound of a word is lost, 
the word cannot be called to mind and cannot be recognized when 
heard. If, having been shown a watch or other familiar object, the 
patient is unable to name it, and does not recognize the correct name 
when stated, he is totally word-deaf, unable to understand what is 
said to him. The lesion is in the middle part of the cortex of the 
first and second temporal convolutions in the left hemisphere in right- 
handed, and in the right hemisphere in left-handed persons. Since the 
patient is unable to call to mind the sound of a word, he is unable to say 
it; but the motor act of pronunciation may be initiated if the impulse 
can be sent to its centre without passing through the auditory centre. 
This is the case in exclamations, when one does not choose his words; 
many patients can swear, although they cannot talk. If the patient 
exhibits recognition of the name of a familiar object when it has been 
stated, he has only partial word-deafness, or auditory amnesia. He 
retains the sound-memory picture (in the cortex), and it can be aroused 
by hearing it (transmission by the auditory tract to the cortex); but he 
cannot make the connection between the sight of the object and the 
sound-memory picture. The lesion, therefore, is subcortical. 

Word-blindness (Alexia, Visual Aphasia). — If the memory of the 
appearance of a word is lost, the usual image of it cannot be called to 
mind or recognized; the patient is therefore unable to read, because the 
shapes of the letters and words seen arouse no recollection, and he is 
unable to write spontaneously, because he cannot remember how the 
letter looks that he wishes to write. Persons who are word-blind can 



842 DISEASES OF THE BRAIN AND SPINAL CORD 

sometimes write at dictation or copy, and yet show no evidence of under- 
standing what has been written; the writing centre has been called into 
activity through some association tract without the intervention of the 
word-memory picture. A distinction must be made between those who 
have lost the memory picture (cortical word-blindness) and those in 
whom it cannot be recalled by ordinary means (subcortical word- 
blindness). Visual amnesia with word-blindness is due to a lesion 
involving the inferior parietal convolutions and angular gyrus in the left 
hemisphere in right-handed persons, and vice versa. It may be associ- 
ated with psychical blindness. Word-deafness and word-blindness fre- 
quently occur together; the lesion involves the temporal convolutions 
and the angular gyrus. 

Optical Aphasia, Transcortical Aphasia, or Intercortical Sen- 
sory Aphasia. — When the association fibers between the memories of 
sight and the memories of sound are severed, a condition of aphasia re- 
sults, which is characterized by an inability to recall the name of a thing 
seen and to picture to the mind the appearance of a thing named; yet 
the name is recognized when heard, and the object is recognized when 
seen. The lesion lies in the long association tract within the temporal 
and occipital lobes. 

Motor Aphasia (Aphemia). — If the memory of the effort needed to 
pronounce a word is lost, a true paralysis of active speech occurs, 
although the muscles may not be weakened. The loss of speech in- 
volves a loss of the power of repeating words after one another, as well 
as of voluntary speech, and is not accompanied by any inability to 
understand spoken or written language. This is the ordinary form of 
motor aphasia and is due to a lesion of Broca's centre in the posterior part 
of the left third frontal convolution in right-handed persons. 

Agraphia. — Loss of the effort memories necessary for writing is 
known as agraphia: the pen cannot be used; copying, writing at dic- 
tation, and voluntary writing, are all lost. The condition is usually asso- 
ciated with motor aphasia. When a word cannot be recalled to mind, 
or read, or mentally enunciated, in the majority of persons it cannot be 
written; but words then can often be written at dictation, if the person 
is one who has written much. Hence, sensory agraphia and motor 
agraphia must be distinguished, the former being a part of word- 
blindness, the latter not at all associated with inability to read. The 
lesion in motor agraphia is not certainly known, though a few facts 
point to the posterior part of the second frontal convolution as the prob- 
able seat of this function. 

Paraphasia, or Intercortical Motor Aphasia; Aphasia of Con- 
duction. — The several memory pictures which are united in the word- 
image may reasonably be regarded as separate from one another in their 
location in the brain. But since they are joined together to form the 
word-image, it follows that the association fibers joining the various 
areas are as necessary to the use of even a single word as the various 
areas with their memories; it is really by association only that an object 



APHASIA 



843 



or a word becomes a subject of thought or use. If these associations are 
broken, the result is a defect of language, characterized by the misplace- 
ment of words, and the patient talks a jargon. There are as many 
phases of this so-called paraphasia, or intercortical aphasia, as there are 
association tracts. In intercortical motor aphasia the patient can under- 
stand what is heard or seen, and can enunciate words clearly, but is 
unable to repeat after another person a word heard; he talks rapidly 
and constantly, trying hard to convey his ideas, but he cannot be under- 
stood on account of the mingling of nonsense words or of syllables with 
words (jargon). 

Some lesion of these association fibers is found at the necropsy in 
almost all cases of aphasia, so that aphasia of purely cortical origin is 
rare. The lesion of these fibers necessarily causes great confusion in the 
mental processes of association, so that defects of intelligence are very 
striking in all cases of aphasia. Marie states that in almost all cases a 
lesion can be shown in the lenticular zone lying at the bottom of the 
Sylvian fissure and outside of the lenticular nucleus — the zone through 
which the majority of these association fibers pass. This he terms the 
" intellectual centre of language." He regards the motor centre in 
Broca's convolution as wholly subsidiary, and he considers that its 
lesion causes anarthria (difficulty in the proper muscular act of speaking 
without disturbance of intelligence) rather than aphasia. Marie's opin- 
ions have not yet been accepted. 

The accompanying table (Starr's) shows the chief defects in each 
variety of aphasia: 



Table IV. — The Symptoms in Different Forms of Aphasia. 



Variety. 


Understand- 
ing of 
language. 


Power to re- 
peat words. 


Power to talk. 


Power to read. 


Power to write. 


1. Word-deafness. 












(a) cortical, 


Lost. 


Lost. 


Retained 
(not to answer). 


Retained 
(not aloud). 


Retained. 


(&) subcortical. 


Lost. 


Lost. 


Imperfect 
(not to answer). 


Retained 
(not aloud). 


Retained. 


2. Word-blindness. 












(a) cortical, 


Retained. 


Retained. 


Retained. 


Lost. 


Lost. 


(6) subcortical. 


Retained. 


Retained. 


Retained. 


Lost. 


Imperfect. 


3. Intercortical, 












between T. and 0. 


Imperfect. 


Retained. 


Retained. 


Imperfect 
(without com- 


Retained 
(not at dicta- 


4. Motor aphasia. 








prehension). 


tion). 


(a) cortical, 


Retained. 


Lost. 


Lost. 


Retained 
(not aloud). 


Lost. 


(6) subcortical. 


Retained. 


Lost. 


Lost. 


.Imperfect 
(not aloud). 


Lost. 


5. Agraphia. 












(a) cortical, 


Retained. 


Retained. 


Retained. 


Retained. 


Lost. 


(6) subcortical. 


Retained. 


Retained. 


Retained. 


Retained. 


Imperfect. 


6. Intercortical, 












between T. and F. 


Imperfect. 


Lost. • 


Jargon. 


Imperfect. 


Lost or im- 
perfect. 



Apraxia, the loss of concepts, includes psychical blindness, psychical 
deafness, amnesia, and astereognosis. 



844 DISEASES OF THE BRAIN AND SPINAL CORD 

Psychical blindness is a condition in which there is a loss of visual 
memories, so that the recognition of objects seen is imperfect and the 
mind cannot recall the appearance of things formerly familiar; the 
members of the patient's family, for instance, may not be recognized by 
sight (optic asymbolia), although they may be identified by the sound of 
their voices ; objects once familiar cannot be named (anomia). The lesion 
in these cases is in the cortex of the occipital lobe, in the convexity (wide 
area of the location of visual memory pictures), as well as in the cuneus; 
commonly in the left hemisphere in right-handed subjects, and vice 
versa. Hemianopsia is usually also present, always when the cuneus is 
destroyed; and word-blindness (really a part of psychical blindness) 
may also be associated, although it may occur without psychical blind- 
ness. 

Psychical deafness (mind deafness) is a condition in which the 
patient loses the auditory memory of sounds, of musical melodies and 
harmonies (amusia), and of words (word-deafness), although he may retain 
the power of hearing; he no longer recognizes sounds or noises, or 
musical melodies or harmonies once familiar, or words once well known. 
The lesion is in the left temporal cortex in right-handed persons, and 
vice versa. 

Amnesia comprises a destruction of the power of memory — an inability 
to recall a whole or a part of past experiences. In some cases the power 
to recall these experiences is only partially lost, lessened, or impeded 
(delayed), a condition spoken of as hypomnesia; or the condition may 
be one of perversion of memory (paramnesia). 

Astereognosis is a condition in which the patient is unable to 
recognize objects by the sense of touch (without the aid of sight). 
The stereognostic sense is a complex made up of tactile, temperature, 
pressure (weight), and other memories; it is represented in the sensory 
area of the parietal cortex, especially in the middle third of the posterior 
central convolution and the adjacent part of the inferior parietal lobule, 
since stereognostic impressions are in greatest number received by the 
hands. Astereognosis, therefore, occurs as a symptom of disease of the 
sensory, cortical, or subcortical area. 

Diagnosis. — Starr states that to examine an aphasic subject thor- 
oughly it is necessary to test: (1) The power to recognize objects seen, 
heard, felt, tasted, or smelled, and their use. This will determine 
whether the condition of apraxia, or disturbance in the power of recalling 
any part of a concept, is present. (2) The power to recall the spoken 
name of objects seen, heard, handled, tasted, or smelled. (3) The 
power to understand speech and musical tunes. (4) The power to 
recall to mind objects named. This will test the integrity of the audi- 
tory speech area and of the association tracts between other sensory 
areas and the temporal convolutions. (5) The power to understand 
printed or written words. (6) The power to read aloud and to under- 
pin. I what is read. (7) The power to recall objects the names of 
which are seen. (N) The power to write spontaneously and to w r rite 



LATERAL SCLEROSIS 845 

the names of objects seen, heard, etc. (9) The power to copy and to 
write at dictation. (10) The power to read understanding^ what has 
been written. These tests will determine the condition of the usual 
word memories in the angular gyrus and of the connections between 
this area and surrounding sensory and motor areas. (11) The power to 
speak voluntarily, and, if it is lost, the character of the defects. (12) 
The power of repeating words after another. This will test the integrity 
of Broca's centre and its association tracts. 



SYSTEM DISEASES OF THE BRAIN AND SPINAL CORD. 

Diseases of the Upper (Central) Motor Neuron. 

LATERAL SCLEROSIS. 

(Spastic Spinal Paralysis, or Paraplegia, of Adults; Spastic Tabes.) 

Lateral sclerosis, or spastic spinal paralysis (Erb), is a primary de- 
generation of the upper motor neuron— that is, of the pyramidal tracts. 

Etiology. — The disease is most common in early adult life — after the 
twentieth year — although an analogous condition may develop in chil- 
dren; and the disorder may be familial. The cause of the disease is not 
known; it has been attributed to infections, especially syphilis. Doubt- 
less there is a congenital weakness (abiotrophy) of the upper motor 
neuron, or some primary nutritional change in the motor cells of the 
cerebral cortex, although some observers doubt whether this ever occurs. 

Pathology. — The lesions consist of degeneration of the upper motor 
neuron, that is, of the pyramidal tracts; this may be confined to the 
cord or may extend to the cerebral cortex. Following the nerve-fiber 
degeneration there is a secondary overgrowth of neuroglia. 

Symptoms. — The symptoms, which usually develop in, and may be 
for a very long time, if not entirely, confined to, the legs, consist of a 
sense of fatigue upon slight exertion, progressive muscular weakness 
and spasticity, and exaggerated reflexes — knee-jerks, ankle clonus, and 
the Babinski sign. The rigidity of the muscles occasions a spastic 
gait, adduction of the thighs (scissors gait), a tendency to stub the toe, 
etc. There is no muscular atrophy, no sensory disturbance, no ataxia, 
and no disorder of the sphincters. 

Diagnosis. — The diagnosis must be made with circumspection, bearing 
in mind that primary lateral sclerosis is very rare. Progressive mus- 
cular weakness and spasticity, increased reflexes, and the Babinski sign 
indicate disorder of the lateral columns, but this may be due to dis- 
seminated or multiple sclerosis, chronic myelitis, vertebral caries, or 
spinal tumor and compression, etc. ; it may be part of a combined system 
disease; it may be secondary to a cerebral lesion, such as apoplexy, 
softening, or tumor; or it may be hysterical. The concomitant symp- 
toms will aid in the diagnosis. 



846 SYSTEM DISEASES OF THE BRAIN AND SPINAL CORD 

Prognosis. — The disease is slowly progressive, and may continue more 
than twenty years (Erb). 

Treatment. — In the primary cases little benefit can be hoped for, 
although massage and passive movements may promote the comfort of 
the patient. Spiller has suggested surgical division of some of the pos- 
terior lumbar roots, with a view to lessen the spasticity, and has had the 
operation done with benefit. 



SPASTIC PARALYSIS OF INFANTS. 

{Cerebral Palsies of Children; Birth Palsies; Spastic Diplegia, or Paraplegia, or 
Hemiplegia of Infants; Spastic Cerebral Paraplegia; Little's Disease.) 

The spastic paralyses of infants and children comprise several groups 
of cases: (1) In most cases the disorder dates from birth; the labor, as 
a rule, was difficult, and forceps perhaps were used. The primary 
lesion consists of a more or less extensive meningeal hemorrhage (usually 
venous), which may be limited to the motor area, but may also extend 
to the frontal lobes (when the intelligence is likely to suffer). Secondary 
sclerosis and non-development of the brain ensue. (2) In another series 
of cases there is more or less extensive agenesis of the brain — convolu- 
tions, a lobe, or a hemisphere — due to imperfect blood supply (hemor- 
rhage, thrombosis, or embolism). There may be associated porencephalus. 
(3) In some cases there is a foetal meningo-encephalitis, which may be 
syphilitic. (4) Other infants are born prematurely, before the pyramidal 
tracts have properly developed, and an arrested development is believed 
to be the cause of the disease (Little's disease). In the different types of 
cases, syphilis, alcoholism, and neuropathies in the parents are looked 
upon as etiological factors. Some cases follow postnatal traumatism to 
the child's head, the infectious diseases, etc. 

Symptoms. — The symptoms vary somewhat with the type of the dis- 
order. In the cases due to injury during birth, paralysis may be notice- 
able during the early days of life, and is likely to be paraplegic (two 
extremities) or diplegic (four extremities). In other cases the child per- 
haps may have had convulsions during early life, but noteworthy symp- 
toms are not manifest until the child should begin to walk, when stiffness 
and inability to use the muscles, especially of the legs, become apparent. 
In still other cases there may be a sudden onset, attended by uncon- 
sciousness and convulsions, and followed by paralysis— which is likely 
to be hemiplegic, sparing the face. When fully developed there is 
paralysis— diplegic or paraplegic; the legs are most commonly involved, 
but the arms also may be affected, and the child may not be able to 
sit up or support its head (involvement of the neck muscles). The 
involved muscles are stiff and rigid; the adductor spasm of the thigh 
muscles causes approximation of the knees or crossing of the legs, and 
impedes or prevents walking. The reflexes are exaggerated; irregular, 
spasmodic movements of the muscles are common, especially on volun- 



AMAUROTIC FAMILY IDIOCY 847 

tary movement (spastic chorea or athetosis, usually bilateral); epilepsy 
is a frequent sequel; the mentality is usually imperfectly developed, and 
imbecility or idiocy may ensue. 

Diagnosis. — The diagnosis is usually apparent from the history of the 
development of the disease and the mentioned symptoms. 

Prognosis. — The outlook is bad, although some improvement in the 
physical and mental condition may be effected by carefully supervised 
physical and educational measures. 

Treatment. — The treatment of the developed disorder comprises general 
hygienic measures, massage, electricity, and orthopedic appliances, but 
they usually avail very little. More attention should be paid to mental 
training, which often results in notable improvement in the mentality of 
the children. Since most of the cases result from meningeal hemorrhage 
during birth, Cushing has advised and practised with good result, 
opening the skull and removing the blood clot soon after birth. 



HEREDITARY SPASTIC SPINAL PARALYSIS. 

(Hereditary Spastic Paraplegia.) 

Hereditary spastic spinal paralysis is a rare disorder, occurring in 
several members of the same family — in one or more generations. The 
conspicuous lesions consist of degeneration of the pyramidal tracts 
throughout the cord, although often most marked in the lower thoracic 
and the lumbar regions. The nature of the disorder is not known; it 
is assumed to be an abiotrophy — imperfect development and deficient 
potentiality of the upper motor neuron, in consequence of which it suc- 
cumbs in early life. The symptoms consist of the development during 
infancy, childhood, or adolescence of muscular rigidity and paralysis, 
involving especially the legs; and increased reflexes, including the 
Babinski sign. There are no sensory disturbances and no disorders 
of mentality. The disorder is usually slowly progressive, and is not 
amenable to any treatment. 



AMAUROTIC FAMILY IDIOCY. 

(Hereditary Spastic Paraplegia — Cerebral Type; Toy-Sachs' Disease.) 

Amaurotic family idiocy is described by Sachs as a family disease of 
infancy of unknown etiology, and of which the basis is "a nervous system 
so inadequate to the demands imposed upon it that its cells, after having 
performed their function for a few weeks or months undergo complete 
disintegration." The condition, therefore, is also an abiotrophy, and is 
akin to hereditary spastic spinal paralysis; both disorders are often 
described as, respectively, the spinal and the cerebral type of hereditary 
spastic paraplegia. The chief symptoms of the cerebral type, or amau- 
rotic family idiocy, are thus summarized by Sachs : Mental impairment 



848 SYSTEM DISEASES OF THE BRAIN AND SPINAL CORD 

during the first months of life, leading to absolute idiocy; paresis, or 
paralysis of the greater part of the body, which may be flaccid or spastic; 
normal, deficient, or increased reflexes; diminution of vision, terminating 
in absolute blindness (the cherry-red spot in the region of the macula 
lutea, and later a simple optic atrophy); marasmus, and a fatal termi- 
nation, as a rule, before the age of two years; the occurrence of the 
affection in several members of the same family; and in some, but not 
all, cases, nystagmus, strabismus, hyperacusis, and convulsions. Since 
the disease has been frequently observed in the children of blood rela- 
tions, Sachs advises discouraging consanguineous marriages, with a view 
to prevent the birth of such amaurotic children. 



UNILATERAL ASCENDING AND UNILATERAL DESCENDING 

PARALYSIS. 

Unilateral ascending and unilateral descending paralyses comprise 
symptom-complexes, first described by Mills, in which unilateral primary 
degeneration of the pyramidal tract (upper motor neuron) occurs, and 
of which the clinical expression is unilateral spastic paralysis, beginning 
as a rule, in the lower extremity and ascending. Mills states that the 
disorder may be a primary degeneration of the pyramidal tracts, or 
may occur in focal disease (tumor or softening) of the brain or cord, in 
multiple sclerosis, in cerebrospinal syphilis, in hysteria, and as unilatera 
amyotrophic lateral sclerosis or paralysis agitans. 



Diseases of the Lowek (Peripheral) Motor Neuron. 

CHRONIC ANTERIOR POLIOMYELITIS. 

(Progressive Spinal Muscular Atrophy; Progressive Muscular Atrophy of the 
Duchenne-Aran and the Vulpian Type.) 

Etiology. — Chronic anterior poliomyelitis, or progressive spinal mus- 
cular atrophy, is most common in middle life (excluding the infantile 
cases). It may develop upon an obsolete acute poliomyelitis (page 270), 
or may be due to syphilis, lead poisoning, etc. 

Pathology. — The lesions consist of degeneration and atrophy of the 
motor nuclei in the anterior cornua of the spinal cord, and corresponding 
atrophy of the motor roots. In some cases there are associated degen- 
erative changes in the pyramidal tracts (amyotrophic lateral sclerosis). 

Symptoms. — The chief symptoms consist of muscular atrophy and 
proportionate weakness and flaccidity (flaccid paralysis), which are 
usually first manifest in the small muscles of one or both hands (Du- 
chenne-Aran type), less commonly in the muscles of the shoulder girdle 
( Vulpian type), and rarely in the muscles of the feet or the trunk There 
air also diminished dr lost reflexes, fibrillary twitchings of the affected 



PROGRESSIVE NEURAL MUSCULAR ATROPHY 849 

muscles, and the reactions of degeneration (partial or complete). The 
atrophy is progressive, and ultimately leads to the development of the 
claw-like hand (main-en-griffe) ; beginning in the hands, it may later 

lplicate the muscles of the forearm, arm, shoulder, and trunk. There 
ire no sensory changes nor involvement of the sphincters. Occasionally 
exacerbations of the process are observed (subacute poliomyelitis). 

Werding and Hoffman have described a similar disorder, beginning in 

Lfancy or childhood, often hereditary, and affecting several members 
of the same family. 

Diagnosis. — The disease should be distinguished from multiple neu- 
ritis (pain and tenderness of the nerve trunks and sensory changes), 
amyotiophic lateral sclerosis (exaggerated tendon reflexes), progressive 
neural muscular atrophy, the muscular dystrophies, syringomyelia, etc. 
Some neurologists distinguish between chronic anterior poliomyelitis and 
progressive spinal muscular atrophy, the chief distinction being the absence 
of periods of exacerbation in progressive spinal muscular atrophy. 

Prognosis. — The disorder is usually progressive, but arrest sometimes 
occurs. 

Treatment. — Massage, electricity, passive movements, tonics, etc., are 
sometimes useful, but commonly avail little. 



PROGRESSIVE NEURAL MUSCULAR ATROPHY. 

(Progressive Muscular Atrophy of the Char cot-Marie-Tooth Type; Peroneal Type of 
Progressive Muscular Atrophy.) 

Etiology. — Progressive neural muscular atrophy is more common in 
males than females; it is often an hereditary or family disease, and 
commonly develops before the twentieth year. No cause is known. 

Pathology. — The lesions consist of degeneration of the axons and con- 
nective-tissue overgrowth of the peripheral nerves, atrophy of the cells 
of the anterior cornua of the spinal cord, degeneration of the posterior 
roots and columns, slight degeneration of the pyramidal tracts, and 
atrophy of the muscle fibers, with connective-tissue overgrowth. 

Symptoms. — The chief symptoms consist of progressive muscular 
atrophy, weakness, and flaccidity (flaccid paralysis), beginning in the 
small muscles of the feet, and later involving the peroneal muscles, so 
that foot-drop ensues. In the course of time the muscles of the thigh may 
become involved, as well as the small muscles of the hands, and perhaps 
the forearm. The muscles of the upper arm, neck, trunk, and face are 
rarely implicated. Associated with the paralyses there are fibrillary 
twitchings of the affected muscles, diminished or lost reflexes, reactions 
of degeneration (partial or complete), and often paresthesia, lessened 
sensibility, and slight pain in the affected peripheral regions. 

Diagnosis. — The hereditary or family occurrence of the disease, its 
development in early life, the almost if not quite complete limitation 
of the atrophic and other changes to the periphery, and the prominence 
54 



850 SYSTEM DISEASES OF THE BRAIN AND SPINAL CORD 

of the motor as contrasted with the sensory phenomena, are character- 
istic of the disease and distinguish it from progressive spinal muscular 
atrophy (chronic anterior poliomyelitis), multiple neuritis, and the mus- 
cular dystrophies. 

Prognosis. — The disease is slowly progressive, but, having reached its 
height, it may remain stationary for years. 

Treatment. — No known treatment is of any noteworthy avail, but 
massage, electricity, passive movements, and orthopedic appliances may 
afford symptomatic relief. 



BULBAR PARALYSIS. 

(Inferior Polioencephalitis.) 

Bulbar palsy is a paralysis of the motor nuclei of the bulb (pons and 
medulla) — that is, the motor trigeminal, the facial, the glossopharyngeal, 
the vagus, the spinal accessory, and the hypoglossal nuclei. 

Acute bulbar palsy (inferior polioencephalitis) may be due to 
acute inflammation (akin to acute anterior poliomyelitis), or to embo- 
lism, thrombosis, or hemorrhage of the vessels supplying the bulbar 
nuclei. The lesions are analogous to those of acute poliomyelitis (page 
270), or to those of embolism, thrombosis, or hemorrhage occurring else- 
where in the brain. The onset is usually sudden, and may be attended 
by headache, vertigo, and vomiting. If death does not soon ensue 
(which is common, on account of respiratory and cardiac failure) the 
muscles of the lower part of the face, the lips, the tongue, the palate, and 
the pharynx are found to be paralyzed. Death may eventually ensue. 
In some cases there is associated ophthalmoplegia (superior polio- 
encephalitis) or acute poliomyelitis. The cases due to hemorrhage or 
softening (embolism or thrombosis) may sometimes be distinguished 
from those due to infection or toxemia (inflammation) by their being more 
sudden in onset, and usually attended by motor (paralytic) and sensory 
phenomena due to implication of the related tracts passing through the 
pons and medulla; and sometimes by the absence of fever and other signs 
of infection. 

Chronic bulbar palsy (glosso-labio-laryngeal and pharyngeal 
paralysis) occurs especially after the fortieth year, and is of unknown 
etiology; it is probably an abiotrophy. The lesions consist of bilateral 
degeneration of the motor nuclei of the bulb, especially the vagus, spinal 
accessory, and hypoglossal. 

Symptoms. — The symptoms consist of the gradual onset and pro- 
gression of difficulty in articulating (hypoglossal involvement), which 
is especially marked in connection with labials, such as b, p, and v, 
and Unguals, such as 1, m, r, and t. Soon there is difficulty in swal- 
lowing (vagus and spinal accessory involvement), and fluids regurgitate 
through the nose (paralysis of the palatal and pharyngeal muscles); 
food may pass into the larynx (loss of the pharyngeal reflex), and the 






OPHTHALMOPLEGIA 851 

voice takes on a nasal quality and becomes weak. In the course of time 
the muscles of the lips (orbicularis oris, supplied by the hypoglossal), 
lower part of the face (facial nerve), and tongue become paralyzed and 
atrophied, and exhibit fibrillary twitchings and the reactions of degener- 
ation; the tongue cannot be protruded; the lips cannot be puckered (as 
in whistling); the saliva drools from the mouth; the palatal, pharyngeal, 
and laryngeal reflexes lessen and finally disappear; and in the course of 
several years the patient dies from respiratory or cardiac failure, if he 
has not earlier succumbed to an intercurrent infection. Intelligence is 
preserved throughout the course of the disease and there are no sensory 
changes. In some cases there is an associated ophthalmoplegia. 

Diagnosis, — The diagnosis is rarely difficult. Some confusion may occur 
with 'pseudobulbar palsy, a disorder caused by supranuclear (cerebral) 
lesions; but in this there is usually a history of apoplectiform attacks, the 
lesions are unilateral or asymmetrical in distiibution and non-progressive 
(in the absence of succeeding apoplectiform attacks), and muscular 
atrophy, fibrillary twitchings, and the reactions of degeneration do not 
occur. So-called asthenic bulbar paralysis, or myasthenia gravis (a dis- 
order of unknown nature, although probably toxic, and muscular rather 
than nervous in origin), may be distinguished by the rapid exhaustion 
of the muscles upon slight exertion, and their recovery upon resting; by 
involvement of muscles other than those innervated by the bulb (such as 
the limbs and the ocular muscles), and the absence of atrophy and fibrillary 
twitchings of the affected muscles; and by the presence of the myasthenic 
reaction (early exhaustion of the muscle, especially when stimulated by 
the faradic current, and recovery after resting). Postdiphtheritic and 
other forms of multiple neuritis and the cases due to tumor, meningitis, 
etc., should be readily distinguished. 

Prognosis. — The disease, as a rule, is steadily progressive. 

Treatment, — There is no satisfactory treatment. Benefit often attends 
general hygienic measures, electricity, and strychnine. Special care 
must be taken in feeding the patient to prevent aspiration of food and 
consecutive bronchopneumonia. 



OPHTHALMOPLEGIA. 

{Superior Polioencephalitis.) 

Ophthalmoplegia, or paralysis of the motor nuclei of the eyeball, is a 
disorder in every way allied to bulbar palsy, with which it is often asso- 
ciated; like it, it may be acute or chronic, and the etiological factors are 
analogous. The acute cases may be sudden in onset, attended by head- 
ache, vertigo, and vomiting, and are characterized by rapidly developing 
paralysis of the ocular muscles — except, in some cases, the elevator of 
the upper lid and the sphincter of the iris. In some cases death ensues 
in stupor or coma; in other cases the patient may recover (usually neu- 
ritic cases), or chronic ophthalmoplegia may ensue. This may also be 



852 SYSTEM DISEASES OF THE BRAIN AND SPINAL CORD 

a chronic process from the beginning, and is characterized by gradually 
progressing paralysis of the ocular muscles, commonly bilateral. The 
paralysis may be partial or complete and may involve one or all the 
muscles. Diplopia is the chief complaint, but it may disappear in 
advanced cases. Ptosis may or may not be present. In some cases 
only the extraocular muscles are involved (external ophthalmoplegia); 
in some cases only the internal muscles (internal ophthalmoplegia); in 
other cases, both. The disorder is usually found in association with 
syphilis, tabes dorsalis, paretic dementia, and progressive muscular' 
atrophy. The treatment is unsatisfactory, but the salicylates seem to 
be of value in some acute cases, and the iodides in some of the chronic 
cases, even in the absence of a history of syphilis; in the event of syph- 
ilis the iodides should be combined with mercury. The chronic cases 
are occasionally benefited by electricity and strychnine; and the diplopia 
may be corrected by glasses. 



Disease of the Upper (Central) and the Lower (Peripheral) 
Motor Neurons. 

AMYOTROPHIC LATERAL SCLEROSIS. 

(Progressive Muscular Atrophy; Charcot's Disease.) 

Etiology. — Amyotrophic lateral sclerosis is a disease of adult life and 
is somewhat more common in men than in women. It is doubtless an 
abiotrophy, but has been attributed 'to intoxications like lead poisoning, 
and to infections, such as syphilis, etc. ; but a definite causal relationship 
has not been shown. 

Pathology. — The lesions consist of degeneration and atrophy of the 
upper and the lower motor neurons — that is, of the pyramidal tracts, 
the nerve cells of the anterior cornua of the spinal cord, the anterior nerve 
roots, the peripheral nerves, and the muscles. The degeneration of the 
pyramidal tracts sometimes extends to the cerebral cortex, involving 
both the axons and the nerve cells. 

Symptoms. — The symptoms consist of a combination of those of 
lateral sclerosis (weakness and spasticity of the muscles of the legs, with 
increased knee-jerks, ankle clonus, and the Babinski sign), and of 
progressive muscular atrophy, beginning in the small muscles of the 
bands, and associated with fibrillary twitching and partial or complete 
reactions of degeneration. In the beginning the symptoms in the legs 
or in the arms may be in the ascendancy, but the atrophy in the course 
of time extends to the forearm and the upper arm and may involve the 
muscles of the trunk (with ensuing kyphosis or lordosis) and the thigh; 
those of the lower leg are usually relatively uninvolved. Sensory phe- 
nomena arc in abeyance, although there may be slight pain. Rarely the 
atrophic and other changes begin in the muscles of the shoulder girdle, 



TABES DORSALIS 853 

or in those supplied by the motor nuclei of the bulb (a type of glosso- 
labio-laryngeal and pharyngeal paralysis). 

Diagnosis. — The diagnosis is to be based upon the co-existence of the 
signs of lateral sclerosis and of progressive muscular atrophy (involve- 
ment of the cells of the anterior cornua of the spinal cord). 

Prognosis. — The disease is slowly progressive and commonly termi- 
nates fatally within one to three or four years. 

Treatment. — Treatment is not of much avail. Symptomatic relief may 
follow the use of electricity, massage, passive movements, strychnine, etc. 



Diseases of the Sensory Neuron. 

TABES DORSALIS. 

(Locomotor Ataxia; Posterior Sclerosis.) 

Etiology. — Tabes dorsalis is almost ten times as common in men as in 
women; it develops usually during the fourth decade of life, but cases 
are occasionally encountered in very young subjects (second decade — 
juvenile cases due to hereditary syphilis), and even about or after the 
sixtieth year. In about 95 per cent, of the cases (Erb) tabes dorsalis 
follows syphilitic infection, developing, as a rule, in from five to twenty 
years after the initial lesion; rarely, it ensues within a year or two. 
Trauma, exposure to wet and cold, infections other than syphilis, ex- 
treme bodily and mental exertion, sexual excesses, etc., are sometimes 
said to be of etiological significance. 

Pathology. — Tabes dorsalis is a disease of the sensory neuron: of the 
dorsal-root fibers (exogenous fibers), and not of the fibers that run from 
one part of the cord to another (endogenous fibers); following primary 
degeneration, secondary sclerosis occurs. The situation of the primary 
lesion has not been positively determined. Obersteiner and Redlich 
have accentuated the importance of inflammation of the dorsal pia- 
arachnoid with involvement of the root fibers, which, as they pierce the 
pia-arachnoid, are poor in myelin and have no neurilemma; Nageotte 
believes the process to originate in a meningoneuritis of the dorsal roots 
centrally to the dorsal ganglia, where they are still covered by the dura 
mater; Starr states that the primary lesion is in the posterior spinal 
ganglia and the ganglia of the cranial nerves. In the spinal cord the 
degenerative and sclerotic lesions are found in the pathway of the dorsal- 
root or exogenous fibers. Most of these enter directly into the postero- 
external column (Burdach); some pass into the gray matter; others 
later run in the postero-internal column (Goll), on account of the 
superior fibers crowding toward the median line those fibres that have 
entered lower down; and they end in the nuclei in the dorsal columns 
of the medulla. Other of these root fibers enter directly into a 
small bundle of fibers (Lissauer's tract) at the apex of the posterior 
cornua and ascending or descending a short distance, enter the cornua, 



854 SYSTEM DISEASES OF THE BRAIN AND SPINAL CORD 

where some of them end; others pass forward to the cells of the ante- 
rior cornua or cross over to the opposite side and enter the antero- 
lateral column. Involving these pathways, the sclerosis usually begins, 
or is most marked, in the lumbar region and commonly decreases from 
below upward; rarely it may begin in the sacral, thoracic, cervical, or 
bulbar regions. Changes are often found in the cranial nerves and 
nuclei, especially the optic and ocular nerves, the pneumogastric, etc.; 
in the motor tracts and anterior horns of the spinal cord (this accounting 
for the muscular atrophy of some cases); and in the cerebral cortex 
(tabo-paralysis; paretic dementia). 

The lesions are commonly described as parasyphilitic rather than 
truly syphilitic, but the radicular meningitis often found and the ready 
demonstration of the Wassermann reaction indicate the essentially 
syphilitic nature of the process. 

Symptoms. — The symptoms are quite variable in their mode of devel- 
opment and in their mutual association. They can perhaps be best 
comprehended by bearing in mind : (1) That they result from dorsal-root 
lesions, and that a dorsal root conveys fibers for epicritic, protopathic, 
and deep sensibility (page 803), as well as fibers composing part of a 
reflex arc; (2) that the disease may begin at varying levels of the cord; 
and (3) that not all the fibers in a dorsal root are diseased at once or to 
the same extent. The disease is sometimes divided clinically into the 
first, incipient, painful, or pre-ataxic stage, the second or ataxic stage, 
and the third or paralytic stage. In practice these are not always 
separable the one from the other. 

The chief symptoms of the early stage of the disease consist of: Sharp 
shooting, fulgurant, or lancinating pains, usually in the legs, rarely in 
the arms (cervical tabes); loss of the deep reflexes, especially the knee- 
jerk (Westphal's sign), and of the Achilles tendon reflex; inequality of 
the pupils and the Argyll Robertson pupil (immobility to light, but 
contraction during convergence and accommodation); and swaying of 
the body, perhaps progressing to falling when the eyes are closed (Rom- 
berg's sign). In some cases complaint is of dull aching, rather than of 
sharp pains, and these being interpreted as "rheumatic," the disease is 
for a long time overlooked. Other patients complain early of various 
paresthetic phenomena — such as numbness or tingling of the feet, a 
sensation as if walking on cotton or eggs, etc.; or of delay or difficulty 
in emptying the bladder; or of loss of sexual power and desire; or of 
transient or permanent diplopia (involvement of the cranial nerves); or 
of gradually increasing dimness of vision (primary optic atrophy); or 
of so-called visceral crises, such as gastric crises (severe epigastric pains 
and vomiting), laryngeal crises (dyspnoea and stridor), renal crises (simu- 
lating renal colic), rectal crises, etc. These symptoms, if they do not 
occur early, are likely to come on later, and in varying combinations. 
Sensory disturbances, as a rule, are readily found early if searched for, 
and commonly consist of segmental hyperthesia or anesthesia, often about 
the chest or abdomen or in the legs and soles of the feet. 



TABES DORSALIS 855 

In the course of time ataxia supervenes : the patient at first experiences 
difficulty in walking in the dark; the Romberg sign will be found upon 
examination, but soon the characteristic ataxic gait supervenes — the foot 
being considerably elevated, thrown out with an ill-controlled jerk and 
brought down with a thud, and an effort being made to control these 
movements by close attention with the eyes. Ataxia may also supervene 
in the arms. About this time hypotonia of the muscles may be observed, 
although it often precedes the ataxia; it consists of abnormal flaccidity 
of the muscles (and sometimes also of the ligaments), so that passive 
movements of the limbs much beyond the normal range are possible, 
although there may be no loss of muscular power. There are varied 
sensory disturbances: the pains and paresthetic phenomena may con- 
tinue; bands of segmental hyperesthesia or anesthesia are common; the 
transmission of painful stimuli and the response thereto are delayed; 
and the deep sensibility, especially the sense of location, becomes im- 
paired. Trophic manifestations also ensue, especially herpes zoster, a 
perforating (usually painless) ulcer of the sole of the foot near the meta- 
tarsophalangeal joint of the great toe, and Charcot's arthropathies — 
painless swelling of the large joints, especially the knee (due to increase 
of fluid, enlargement and exostosis of the ends of the bones, and 
atrophy and absorption of the bone and the articulating cartilage). 
The bones may become brittle and readily fractured. 

After some years, if the patient does not sooner die, the third, or para- 
lytic stage, develops: the patient, in addition to being ataxic, becomes 
muscularly weak, unable to walk, and finally bedridden. 

In a certain proportion of the cases tabes becomes associated with 
general paralysis of the insane (general paresis, paralytic dementia), 
giving rise to a condition sometimes spoken of as tabo-paralysis. Some 
writers maintain the essential etiological (syphilitic) and pathogenetic 
identity of the two disorders, and believe that the one or the other may 
be the antecedent or the secondary disorder in a given case. The ma- 
jority of cases of tabes dorsalis, nevertheless, are devoid of noteworthy 
mental symptoms, and general paretic subjects, as a rule, are not tabetic. 
However, in some cases of tabes, after the lapse of time, evidences of 
cerebral disorder (chronic meningo-encephalitis) supervene: the subject 
becomes irritable; his character changes, he becomes intemperate, licen- 
tious, and neglectful of himself, his family, and his business; and his 
memory fails. Soon mental deterioration becomes more marked, the 
general condition being that of exaltation and well-being and delusions 
of grandeur, or there may be alternating periods of exaltation and of 
depression. In addition there are disturbances of speech, which be- 
comes slowed; there is special difficulty in pronouncing labials and 
Unguals; tremors of the lips, tongue, face, and hands (especially obvious 
in attempting to write) become noticeable; and the patient gradually 
develops a general muscular weakness, although the mental disorder 
may lead him to deny any bodily infirmity. Transient paralyses, in- 
volving the cranial nerves, or hemiplegia, attacks of stupor, coma, or 



856 SYSTEM DISEASES OF THE BRAIN AND SPINAL CORD 

momentary loss of consciousness, convulsive seizures, especially of the 
face or arm, may supervene. Finally the dementia becomes aggra- 
vated, the patient takes permanently to his bed, and ultimately dies. 
The significant symptoms of tabes are variously associated with these 
manifestations of the cerebral disorder. 

Diagnosis. — The diagnosis of tabes dorsalis should be readily made by 
attention to the aforementioned symptoms. Efforts should be made 
to recognize the disease in its earliest stage; the presence of any two of 
the following signs is of the greatest diagnostic importance: lightning 
pains, Argyll Robertson pupil, lost knee-jerks and other deep reflexes, and 
Romberg's sign; and any one of these in association with two of the other 
mentioned symptoms warrant the diagnosis. In doubtful cases a history 
of syphilitic infection, a positive Wassermann reaction, or an excess of 
lymphocytes in the cerebrospinal fluid, will furnish material diagnostic 
aid. Multiple neuritis should be readily excluded by the absence of 
motor paralysis, muscular atrophy, tender nerve trunks, etc. 

Prognosis. — The disease may pursue a slow or a comparatively rapip 
course, and, having made more or less progress, it may come to a 
standstill. Slow progression in the past is a promise of slow progress 
in the future. The existence of lightning pains for years prior to the loss 
of knee-jerks augurs slow progression or standstill, and the cases with 
early optic atrophy are likely also to show delayed onset of ataxia and 
slow progression of the other symptoms. Degeneration of the columns 
in the spinal cord, once effected, of course, cannot be remedied. 

Treatment. — If the patient is in good physical condition and the disease 
is not far advanced, a course of efficient antisyphilitic treatment should 
be instituted, especially if the infection were poorly, or not all, treated. 
Otherwise, attention should be directed to improving the general nutri- 
tion of the patient by good food, rest, and tonics, such as iron, quinine, 
and strychnine, and hydropathic measures, massage and electricity. 
Arsenic and silver nitrate have been recommended. The lightning pains 
may be benefited by aspirin, acetphenetidin, and other coal-tar deriva- 
tives, aluminum chloride, codeine, and morphine (which are almost 
certain to engender the habit). The ataxia may be markedly improved 
by exercises — which have been systematized for the tabetic subject by 
Fraenkel. 



INTERSTITIAL HYPERTROPHIC PROGRESSIVE NEURITIS OF 

CHILDHOOD. 

Interstitial hypertrophic progressive neuritis of childhood is a heredi- 
tary or familial disorder, studied especially by Dejerine, that develops in 
childhood or adolescence from unknown causes, although it has been 
attributed to syphilis. The chief lesions consist of degeneration of 
the posterior roots and columns of the cord (as in tabes dorsalis) and 
of parenchymatous and interstitial changes in the peripheral nerves, 









HEREDITARY OR FAMILY CEREBELLAR ATAXIA 857 

especially of the legs. The symptoms consist of those of tabes, especially 
ataxia of the arms and legs, severe pains, sensory disturbances (as in 
tabes, with retardation of the appreciation of painful stimuli), inequality 
of the pupils, Argyll Robertson's sign, etc.; general muscular atrophy, 
especially marked at the periphery; and kyphoskoliosis (due to weak- 
ness of the trunk muscles). The palpable nerve trunks are thickened 
and indurated. There is no satisfactory treatment. 

Combined System Diseases. 

HEREDITARY OR FAMILY ATAXIA. 

{Friedreich's Ataxia.) 

Etiology. — Friedreich's ataxia is a family disease, that may or may not 
have occurred in the antecedents. It is slightly more common in males 
than in females, and is likely to develop in early life — often in childhood, 
and in the great majority of cases before puberty. The cause is not 
known. Alcoholism and syphilis in the parents seem to be inoperative. 
Evidently the disease is an abiotrophy. 

Pathology. — The lesions consist of degeneration and consequent scle- 
rosis of the posterior, lateral, and direct cerebellar tracts, and sometimes 
also of Gowers' anterolateral tracts. 

Symptoms. — The symptoms consist of the gradual development during 
early life of ataxia. This occurs first in the legs, and gives rise to a 
swaying or stumbling gait, which usually becomes aggravated on closing 
the eyes (Romberg's sign); developing later in the arms, it occasions 
irregular choreiform movements. The head also may be subject to 
similar movements; and irregular, oscillatory movements may affect the 
body when it is erect at rest, or a limb when it is extended (static ataxia). 
Nystagmus and a slow scanning or stumbling speech often supervene. 
The deep reflexes are lost; the skin reflexes are usually preserved; there 
are no noteworthy sensory changes. In advanced cases, on account of 
muscular weakness and atrophy, talipes equinus, hammer-toes, or spinal 
curvature may occur. 

Diagnosis. — The diagnosis should be quite apparent from the onset of 
the aforementioned symptoms in early life, especially if several members 
of a family are affected 

Prognosis. — The disorder is slowly progressive. 

Treatment. — No satisfactory treatment is known; the available treat- 
ment is purely symptomatic. 

HEREDITARY OR FAMILY CEREBELLAR ATAXIA. 

{Marie's Ataxia; Hereditary or Family Spastic Paraplegia.) 

Hereditary or family cerebellar ataxia is a family disorder, that tends 
to develop after puberty or in early adult life (the third decade), and is 
characterized anatomically by gross atrophy of the cerebellum or by 



858 SYSTEM DISEASES OF THE BRAIN AND SPINAL CORD 

microscopic atrophy of the cells of Purkinje. Clinically, the disorder 
resembles Friedreich's ataxia in the family occurrence, the ataxia 
(although the gait is likely to be less awkward), the Romberg's sign, 
the choreiform movements, the nystagmus, and the disturbances of speech ; 
but it differs from Friedreich's ataxia in its onset later in life, normal or 
exaggerated knee-jerks, ultimate spasticity of the legs (attributable to 
degeneration of the pyramidal tracts), and the absence of deformities of 
the feet and trunk. 

ATAXIC PARAPLEGIA. 

(Posterolateral Sclerosis.) 

Etiology. — Ataxic paraplegia occurs most commonly in males in the 
fourth and fifth decades. No cause can be assigned; it is not due to 
syphilis; it has been attributed to cold and wet, traumatism, etc.; it is 
probably an abiotrophy. 

Pathology. — The lesions consist of degeneration and consequent 
sclerosis of the posterior and the lateral columns; that of the posterior 
columns differs from that of tabes in being equally marked in the lumbar 
and thoracic regions and in sparing the dorsal -root zones; that of the 
lateral columns is most marked in the pyramidal tracts, but may also 
involve the direct cerebellar and the direct pyramidal tracts. 

Symptoms. — The symptoms consist of gradually developing weariness, 
muscular weakness, and difficulty and unsteadiness in walking. Ex- 
amination reveals well-marked incoordination (as in tabes dorsalis), 
which may extend to the arms; and Romberg's sign. The deep reflexes 
are exaggerated, including ankle clonus and the Babinski sign. In the 
course of time rigidity and spasticity of the muscles of the legs ensue 
(spastic paraplegia), and may somewhat overshadow the ataxic phe- 
nomena. Sensory and ocular symptoms are rare. Late, the sphincters 
may become involved, and mental symptoms, suggesting paretic dementia, 
may develop. 

Diagnosis. — The disease should be readily recognized from the ataxic 
gait, the increased knee-jerks, and muscular rigidity, and the absence of 
the lightning pains, sensory changes, and ocular signs of tabes. 

Prognosis. — The disease is slowly progressive, as a rule, but sometimes 
arrest occurs. 

Treatment. — The treatment is that of primary lateral sclerosis (page 
845), plus Fraenkel's method for the reeducation of muscles, useful in 
tabes dorsalis. 

TOXIC COMBINED SCLEROSIS. 

(Subacute Combined Sclerosis of the Spinal Cord, Putnam; Diffuse Secondary De- 
generation of the Spinal Cord; Anemic Degeneration of the Spinal Cord.) 

Etiology. — The disorder, or disorders, comprised within the term toxic 
combined sclerosis of the spinal cord occur secondarily in the course of 
toxic and anemic conditions, such as pernicious anemia, severe secondary 



MULTIPLE SCLEROSIS 859 

anemias, cachectic conditions generally, acute and chronic infections, 
prolonged suppuration, lead poisoning, ergotism, pellagra, etc. 

Pathology. — The lesions consist of degeneration and sclerosis of the 
posterior columns, usually most marked in the thoracic and cervical 
regions; and sometimes also of the crossed pyramidal tracts; rarely of 
other tracts. The degeneration is sometimes focal rather than systemic. 

Symptoms. — The symptoms consist of early numbness and tingling of 
the feet and legs and mild spastic or ataxic paraplegia. Similar phe- 
nomena may develop in the arms, and those in the legs become aggra- 
vated, so that the patient then exhibits the phenomena of well-marked 
spastic paraplegia, with diminution or loss of all forms of sensibility in 
the legs and perhaps the lower part of the trunk. Finally, a stage of 
flaccid paralysis may supervene. 

Diagnosis. — The development of the mentioned symptoms in the 
course of any of the diseases that may occasion them should serve for 
the diagnosis. 

Prognosis. — The outlook depends more upon the primary disorder 
than upon the nervous manifestations. As a rule, a fatal outcome 
supervenes within a few months. 

Treatment. — The treatment is wholly that of the primary disorder. 

NON-SYSTEM DISEASES OF THE BRAIN AND 

SPINAL CORD. 

MULTIPLE SCLEROSIS. 

(Disseminated Sclerosis; Insular Sclerosis.) 

Multiple or disseminated sclerosis is a disorder characterized by 
small islets or foci of sclerotic neuroglial tissue scattered irregularly 
throughout the brain and spinal cord. 

Etiology. — Multiple sclerosis occurs especially in early adult life (be- 
fore the thirtieth year); it affects the sexes about equally. The exciting 
cause is not known. Some cases are believed to be congenital — an 
abiotrophy; others appear to follow some of the infectious diseases 
(typhoid fever, scarlet fever, smallpox, pneumonia, etc.), and still others 
are attributed to metallic poisons (lead, mercury, etc.). 

Pathology. — The lesions consist of foci or islets of sclerotic neuroglial 
tissue scattered throughout the brain and spinal cord, and sometimes also 
in the peripheral (especially the cranial) nerves. They are much more 
common in the white than in the gray matter, and they vary in size from 
those microscopic to those 3 to 5 mm. or more in diameter. The primary 
lesion seems to be a neuroglial proliferation (perhaps toxic in origin), 
with consecutive destruction of the medullary sheaths of the neurons. 
The lesions are not systemic (that is, not confined to definite tracts) ; and 
sparing, at least for a very long time, the axons, they do not give rise to 
secondary degenerations of tracts or fibers. 

Symptoms. — The onset of the symptoms is insidious and their progress 
slow, and they vary extraordinarily with the seat of the lesions. In the 



860 NON-SYSTEM DISEASES OF THE BRAIN AND SPINAL CORD 

so-called typical cases the early complaint may be stiffness and weakness 
of one or both legs, rarely of an arm. Gradually spastic paralysis of 
the legs develops and is associated with increased knee-jerks, ankle 
clonus, and the Babinski sign; the deep reflexes of the arm also are 
usually increased, but the superficial reflexes, especially of the abdomen 
and the cremasteric reflex, may be abolished. In most cases there is 
more or less ataxia and a staggering gait (involvement of the posterior 
and cerebellar tracts). Muscular tremors develop — usually first and 
most markedly in the arms, but they may involve the legs and the 
head. They are characterized by being absent or ceasing during rest, by 
developing upon voluntary motion of any kind, such as writing, taking 
hold of an object (so-called volitional or intention tremor), by their general 
coarseness, and by increasing in amplitude, jerkiness, and irregularity 
upon continuation of the voluntary movement. Nystagmus is common 
and may develop spontaneously or only upon voluntary movement of 
the eyes; it may be associated with weakness of one or more ocular 
muscles and diplopia. Optic atrophy is often present and is rather 
commonly confined to the temporal half of one or both disks. The 
pupils usually react normally to light and in accommodation. There is, 
in most cases, more or less disorder of speech, which is commonly slow, 
scanning, staccato, syllabic, and in a monotone. Mental impairment 
ensues to a greater or less degree, and the patient becomes emotionally 
unstable, laughing or crying upon little or no provocation. 

There are a number of other symptoms that occur variously in dif- 
ferent cases, such as vertigo, apoplectiform or epileptiform attacks, pares- 
thesias, patchy anesthesias, disorder of the vesical and rectal sphincters, 
etc. The disease is often characterized by notable improvement or dis- 
appearance of some of the obtrusive symptoms and by relapse or recur- 
rence. 

Diagnosis. — A combination of the symptoms mentioned is quite char- 
acteristic. In the early and ill-developed cases (especially in young 
women) care must be taken not to confound the disease with hysteria; 
in hysteria, however, intention tremors, nystagmus, optic atrophy, scan- 
ning speech, and the Babinski sign are absent, and various hysterical 
stigmas are likely to be present. Cerebrospinal syphilis may simulate 
multiple sclerosis, but it is likely to exhibit pupillary and other phe- 
nomena, and rarely, if ever, shows intention tremors, nystagmus, and 
scanning speech. Paralysis agitans also is characterized by a tremor, 
but this occurs while the parts are at rest and is fine, nystagmus and 
scanning speech are absent, and the disease occurs in advanced life. 
Friedreich's and cerebellar ataxia should be readily excluded. 

Prognosis. — The disease is of slow progress; remissions are quite 
common; standstill may ensue, but recovery is not likely. 

Treatment. — The treatment is symptomatic: rest, the avoidance so far 
as possible of muscular movements (talking, walking, exercise, etc.), 
warm baths, massage, electricity (galvanism), and tonics, such as iron, 
quinine, arsenic, etc. 






ANEMIA OF THE BRAIN 861 

DIFFUSE AND FOCAL DISEASES OF THE BRAIN. 
HYPEREMIA OF THE BRAIN. 

Active hyperemia of the brain occurs in the many and varied condi- 
tions that increase the force and rapidity of the heart's action, especially 
the acute infectious diseases, alcoholism and other intoxications, pro- 
longed mental strain, and emotional disturbances; and it is a part of 
sunstroke, meningitis, and encephalitis. Although in these circum- 
stances more blood passes through the brain in a given time, it is not 
definitely known that more than a normal amount is present at any one 
time (on account of the relative inexpansibility of the brain and the 
absence of local vasomotor control); nor is it likely that the condition 
of itself gives rise to any noteworthy symptoms; the cerebral symptoms 
that do occur are much more likely due to the initiating infectious or 
toxic factor. 

Passive hyperemia of the brain occurs in conditions of general venous 
engorgement, such as develop in failure of the heart induced by any 
cause (myocardial, endocardial, pericardial, or chronic pulmonary dis- 
ease), and local conditions, such as venous or sinus thrombosis, tumors 
and abscess of the brain, and tumors, aneurysms, and other factors 
obstructing the circulation in the neck. The symptoms consist of head- 
ache, with a feeling of general tenseness and perhaps pulsation, and of 
pressure behind the eyes, vertigo, tinnitus aurium, mental irritability 
and incapacity, etc. The diagnosis should always be made with cir- 
cumspection, since the symptoms mentioned are more likely to be due 
to some cause (toxic?) other than mere congestion; and, assuredly, in 
the chronic cases. The treatment of such cases as may be recognized con- 
sists of attention to the underlying causative factor; the use of general 
depletive measures, especially calomel, or blue mass and saline cathartics, 
hot foot baths, count erirritation to the back of the neck; an ice-cap to the 
head; and the administration of the bromides, ergot, etc. 



ANEMIA OF THE BRAIN. 

Anemia of the brain may result from: (1) Acute or chronic, primary 
or secondary, anemia. The symptomatology and treatment are men- 
tioned on page 365 et seq. (2) Disorder of the vasomotor influences 
acting in the splanchnic area and the skin. When, for instance, the 
vasomotor centre becomes inhibited, as may happen under the influ- 
ence of emotions, or when it becomes of lessened functional activity, as 
may occur in infectious and toxic processes, the circulation in the brain 
may become readily disturbed. In the first mentioned case the abdom- 
inal vessels dilate, and the general blood pressure in consequence falling, 
the heart is no longer able to maintain an efficient circulation in the 



862 DIFFUSE AND FOCAL DISEASES OF THE BRAIN 

brain, cerebral anemia ensues, and the patient faints; in the second 
mentioned case, a satisfactory cerebral circulation may be maintained 
in the recumbent posture, but sudden exertion, emotional disturb- 
ances, or the assumption of the sitting or erect posture, may similarly 
induce cerebral anemia and fainting. A like result may also follow the 
sudden liberation of excessive intra-abdominal pressuie — withdrawal of 
ascites, removal of an abdominal tumor, etc. The treatment consists of 
the recumbent posture (to favor the ready access of blood to the brain) 
and the use of diffusible stimulants. (3) Localized anemia of the brain 
may occur in arteriosclerosis and in what may be interpreted as a condition 
of angiospasm; foci of temporary stasis of the blood are doubtless often 
associated. The symptoms consist of momentary inability to perform 
special cerebral acts, depending upon the area involved, such as think, 
speak, see, move certain muscles, etc. (page 482). These may or may not 
be associated with temporary (momentary) loss of consciousness. The 
conditions have been likened to intermittent claudication (page 493). 
The treatment is that of arteriosclerosis (page 493). 



(EDEMA OF THE BRAIN. 

(Edema of the brain may occur: (1) In conditions associated with 
passive congestion; (2) in chronic nephritis, in which the oedema may 
be widespread or localized, is doubtless toxic in nature, and is answer- 
able for some of the uremic manifestations; (3) in traumatic disorders, 
such as concussion and contusion; (4) about abscesses and tumors; 
and (5) in congenital atrophic disorders, in which the oedema and in- 
creased cerebrospinal fluid fills up potential spaces. The symptoms, 
except in chronic nephritis, are due to associated conditions rather than 
to the oedema per se. 



CEREBRAL HEMORRHAGE. 

(Apoplexy; A Stroke; Hemiplegia.) 

Etiology. — Hemorrhage into the substance of the brain is most com- 
mon in male subjects after the fortieth year. The etiological factors are 
those of arteriosclerosis (page 489), especially syphilis, chronic alcoholism, 
chronic nephritis, excessive muscular work, plumbism, gout, diabetes, 
etc. The exciting cause of the hemorrhage is often some undue increase 
of blood pressure, such as may be provoked by exertion (running, lifting 
heavy bodies, straining at stool, etc.), or emotional disturbances; but in 
many cases the rupture of the bloodvessel occurs during quietude (as 
sleep) — in which event one may assume that the gradually weakened 
vessel finally becomes unable to sustain the ordinary blood pressure 
of that individual. Cerebral hemorrhage, however, may occur into 
tumors; it may develop in conditions of blood dyscrasia, such as per- 



CEREBRAL HEMORRHAGE 



863 



nicious anemia, leukemia, purpura, scurvy, septicopyemia, etc.; and 
occasionally it is observed in children. 

Pathology. — In about three-fourths of the cases the hemorrhage occurs 
from one of the several branches of the middle cerebral (sylvian) artery, 
which, penetrating the anterior perforated space, supply the corpus 
striatum and the internal capsule, especially the lenticulostriate branch 
(Duret's artery; Charcot's artery of cerebral hemorrhage) and the len- 
ticulothalamic branch (Fig. 22). In about one-fourth or more of the cases 
the hemorrhage occurs variously from any of the many branches of the 
cerebral arteries, and into the brain cortex, the peduncles, the pons, the 
medulla, or the cerebellum. The lesions consist of the ordinary changes 
of advanced arteriosclerosis (page 489); small, so-called miliary aneurysms 
are common, and rupture of these is the usual cause of the bleeding. 
Rarely, as in toxic states and the various blood dyscrasies, there may 
be an undue permeability of the vessel walls and an undue fluidity of the 



Fig. 22 




The distribution of the bloodvessels to the internal capsule: E, the lenticulostriate arteries 
(external arteries of the corpus striatum). /, the lenticulothalamic arteries (the internal arteries 
of the corpus striatum). (Duret.) 

blood. The hemorrhage may be large or small ; in most cases it is large 
enough to destroy the outer portion of the lenticular nucleus, the internal 
capsule, and the thalamus; but it may extend to the caudate nucleus and 
the insula, and in extreme cases it may involve almost, if not quite, all 
of the hemisphere and invade the lateral ventricles. In other cases the 
hemorrhage may be small — pinhead in size, for instance — but such a 
small hemorrhage, if occurring in the pons or medulla, may be attended 
by very serious consequences, even death. The blood, soon after being 
poured out, clots; ultimately the clot may be entirely absorbed, and 
represented by a scar, or a cyst may be the residual manifestation. 
Secondary degeneration of those fibers of the upper motor neuron 
deprived of continuity with their cell bodies in the cerebral cortex ensues. 
Symptoms. — In a few cases symptoms described as premonitory are 
noted. Men of an apoplectic habitus (short, rather stout body, with a 
short, thick neck, prominent arteries, and ruddy complexion) are still 



864 



DIFFUSE AND FOCAL DISEASES OF THE BRAIN 



believed by some persons to be predisposed to cerebral hemorrhage; but 
the question is solely one of the cerebral arteries and the mode of life. 
In these, as well as other subjects with sclerotic vessels and high blood 
pressure, there may be attacks of headache, vertigo, and transitory inca- 
pacities (mentioned on page 862); or slight paresis or paralysis involving 
the cranial nerves (especially ptosis, strabismus, or disturbances of 
vision), and due perhaps to small hemorrhages, may ensue; or actual 




Scheme of the motor tract to show the effect of hemorrhagic or softening (thrombotic or 
embolic) lesions at different positions: 1, cortical or subcortical lesion, causing monoplegia of 
the left arm; 2, capsular lesion, causing left hemiplegia; 3, crus lesion, causing left hemiplegia 
and right third nerve palsy; 4, pons lesion, causing alternating paralysis of the right face and 
the left arm and leg; S, sylvian fissure; OT, optic thalamus; NL, lenticular nucleus; C, crus; 
NC, caudate nucleus; VII, facial nerve; M, medulla. (Starr.) 

hemorrhages may be detected in the retina; or paresthetic phenomena 
(numbness and tingling), or choreiform or other movements may occur 
in an arm or a leg. 

In the great majority of cases, however, the apoplectic attack comes 
on suddenly, without warning, The patient, in apparently good health, 
while sitting quietly, or walking, or after some exertion or emotion, sud- 
denly becomes dizzy and falls to the ground unconscious; he may vomit 
and exhibit some convulsive movements. In the usual cases, those due 
to hemorrhage from the lenticulostriate artery or into the internal capsule 
(Fig. 23), and in any event if the hemorrhage is of at least moderate size, 



CEREBRAL HEMORRHAGE 865 

the patient is soon found to have a livid or ashen-gray countenance, 
bathed in sweat, a full, bounding, rather infrequent pulse under increased 
pressure, and a normal or subnormal temperature; to be breathing 
slowly or stertorously, and "flapping" one cheek (paralysis), or exhibiting 
the Cheyne-Stokes rhythm; and to be paralyzed on one side of the body, 
which, however, may be difficult to determine on account of complete 
muscular relaxation. In addition, the head and the eyes may be turned 
toward the side of the lesion in the brain (paralytic conjugate deviation) ; 
the pupils are likely to be unequal or dilated (especially on the side of 
the lesion), and to be inactive to light if the patient is in deep coma; 
and control over the vesical and rectal sphincters may be lost. In some 
cases the paralysis and other phenomena are noted only when the patient 
awakes in the morning; or, not awakening, he is found to have died of 
apoplexy during the night. In other cases the onset is slower: there 
may be at first only headache and vertigo, and perhaps vomiting, with 
gradual loss of power in the arm and leg; but in the course of a few 
hours or a day unconsciousness supervenes and deepens into coma — 
so-called ingravescent apoplexy, due often to slow leakage of blood 
into the external capsule, and its gradual breaking through into the 
internal capsule and perhaps the lateral ventricle. 

One of several eventualities may ensue : (1) The patient may die soon, 
or within several hours of the onset of the apoplexy. (2) The coma 
may continue, or it may lessen somewhat and become associated with 
delirium and fever — 102° to 104° (so-called febrile reaction) — and then, 
recurring, the patient may die at the end of a week or thereabouts. In 
some of the cases, neither improving much nor retrograding, a sudden 
increase of the symptoms may occur; muscular rigidity and perhaps 
convulsions may ensue, and spasmodic conjugate deviation of the head 
and the eyes away from the side of the lesion may supervene. In some 
of these cases sudden inundation of the ventricles is answerable for the 
finally fatal symptoms. (3) With more or less return of consciousness, 
although not complete mental clearness, fever may set in; trophic 
changes may ensue, especially bed sores and sloughing on the paralyzed 
side; congestion of the bases of the lungs (in some way related to the 
cerebral disorder) may supervene; and with bronchopneumonia or 
septicopyemia the patient may die in two or three weeks. (4) The 
coma may gradually subside and the paralysis become obtrusive. This 
is unilateral, and may involve the leg, arm, and one-half of the face and 
tongue (complete hemiplegia), or only one of these parts (sometimes 
called partial hemiplegia). The paralysis at first is flaccid, and is asso- 
ciated with lessened or absent deep reflexes; soon an early rigidity may 
develop and be associated with increased reflexes and the Babinski sign. 
The speech is indistinct; aphasia (page 840) may occur in left-sided 
lesions. There may be slight or no sensory phenomena. 

Hemorrhage into the crus gives rise to paralysis of the face, arm, and 
leg of the side opposite the lesion, and paralysis of the oculomotor nerve 
of the same side (syndrome of Weber; crossed or alternate hemiplegia). 
55 



866 DIFFUSE AND FOCAL DISEASES OF THE BRAIN 

There may also be contralateral hemianesthesia from extension to the 
tegmentum. 

Hemorrhage into the pons and medulla is usually fatal within a few 
hours; but, if the patient survives, there is likely to be convulsions, deep 
coma, contracted pupils, and high fever; and in many cases bilateral 
paralysis, because of involvement of both motor tracts. If the hemor- 
rhage is small, there is contralateral hemiplegia and homolateral dis- 
turbance with the functions of the nerve nuclei therein located (crossed 
hemiplegia); loss of sensation in the area of trigeminal distribution; 
paralysis of the muscles supplied by the facial nerve; or the phenomena 
described under acute bulbar paralysis (page 850). 

Hemorrhage into the cerebellum gives rise to few symptoms significant 
in themselves. Coma, convulsions, and vomiting are common; par- 
alysis may result from pressure on the nuclei or tracts in the medulla 
or pons; characteristic symptoms, such as vertigo, staggering gait, and 
inability to maintain muscular balance and the erect posture, can 
scarcely be ascertained. Death usually ensues. 

Occasionally, after the lapse of several weeks all evidences of the 
apoplexy and paralysis have disappeared and the patient appears to be 
as well as before the attack. In the majority of cases, however, at the 
end of a month or six weeks the patient exhibits the permanent results 
of the hemorrhage — the secondary symptoms, or the chronic stage. As 
a rule, the paralysis is less than at first; some power has returned in 
the arm and the leg — in the leg first, and to a greater degree; the par- 
alysis of the face and the tongue and any sensory disturbances originally 
present may have wholly disappeared. In the usual cases (hemorrhage 
into the internal capsule), however, more or less unilateral paralysis of 
the upper motor neuron type persists. This is most marked in the arm 
and the leg; muscles that act bilaterally, such as those of the face 
(wrinkling the forehead, frowning, closing the eyes) and of the trunk 
(respiration, etc.), are likely to show relatively slight impairment of 
function, since they doubtless may be innervated by stimuli from one 
side of the brain; and movements associated with emotional disturbances 
(langhing and crying) also are usually well executed, although the 
patient may not be able voluntarily to move the angle of his mouth. In 
addition, rigidity (so-called late rigidity) of the affected muscles develops 
and usually progresses to deformities (contraction of the flexors and adduc- 
tors overcoming the extensors and abductors); in walking, the great toe 
is dragged along the ground, and the leg, as a whole, circumducted 
(swung on an arc of a circle from the hip); the deep reflexes are exag- 
gerated, and ankle clonus and the Babinski sign become apparent; there 
is little, if any, wasting of the muscles aside from what may be attributed 
to disuse. Sometimes there is persisting hemianesthesia (involvement of 
the t posterior part of the internal capsule), and rarely pain (irritation of 
the sensory neuron). Athetoid and choreiform movements may develop 
in the paralyzed limbs (posthemiplegic chorea and athetosis). In most 
cases there is at best slight impairment of mentality; in many cases 



CEREBRAL HEMORRHAGE 867 

mental irritability, emotional disturbances on slight provocation, failure 
of memory, etc., supervene, and dementia may occur. 

Diagnosis. — At the time of the apoplectic attack one must differentiate 
it from coma due to other causes, such as: (1) Embolism and throm- 
bosis. Apoplexy is often employed as an inclusive term, comprising 
hemorrhage and softening (embolism and thrombosis); but thrombosis 
is suggested by gradual onset of the paralysis and coma, both of which 
may be transitory; by a history of syphilis or of another infection recently 
passed through; and by conditions of the blood generally that favor 
clotting. Embolism is suggested by a young subject and vegetative 
endocarditis or other disorder whence an embolus may be derived. (2) 
Uremia. Renal disease (cardiovascular-renal disease) is often pres- 
ent in those the subject of apoplexy, so that it may be difficult to 
make a differential diagnosis; but uremia is suggested by albumin and 
casts in the urine, convulsions, very high blood pressure, albuminuric 
neuroretinitis, the absence of hemiplegia, and a history of previous 
attacks without consecutive paralysis. But now and then fatal cases of 
hemiplegia are encountered in which only nephritis and oedema of the 
brain and meninges are found at the necropsy. (3) Diabetic coma — 
which may be distinguished by ketonuria, perhaps glycosuria, fruity odor 
to the breath, the characteristic Kussmaul dyspnoea, and the absence of 
hemiplegia. (4) Alcoholic coma (obvious alcoholism, alcoholic habits, 
less deep coma, and absence of hemiplegia or other localized paralysis). 
(5) Opium poisoning (contracted pupils, infrequent respirations, no 
convulsions, no paralysis). 

Prognosis. — Death may occur on the first attack, but recovery, with 
more or less permanent incapacity, frequently ensues. Succeeding attacks 
are likely to occur, and with each the tendency to fatality increases. 

Treatment. — It is important, first, to determine whether the " apo- 
plexy" is due to hemorrhage or to thrombosis or embolism. In hemor- 
rhage the patient should be kept quiet, with the head high and the neck 
free. If breathing is obstructed, he should be turned on his side, to 
obviate obstruction of the pharynx by the paralyzed tongue. To reduce 
the blood pressure and promote stilling the bleeding, ice may be applied 
to the head and hot bottles to the feet, or a hot mustard foot bath may 
be given; and venesection should be performed; or one may give 
aconite, veratrum viride, or nitroglycerin, and open the bowels freely 
(calomel, croton oil, eletarium). But Crile and Cushing have shown 
that a high arterial pressure may be conservative, inasmuch as this tends 
to supply a sufficiency of blood to the vital centres in the medulla, which 
otherwise — that is, under the influence of a rising intracranial pressure — 
would rapidly become anemic and exhausted. Therefore, in cases 
with marked and rising blood pressure (250 mm. Hg. — indicative of 
increasing intracranial pressure), especially if associated with an infre- 
quent pulse, Cushing recommends, and has practised with good results, 
trephining the skull and evacuating the blood clot. This is particularly 
indicated, of course, in meningeal hemorrhage, but it has been sue- 



868 DIFFUSE AND FOCAL DISEASES OF THE BRAIN 

cessfully done in cerebral hemorrhage. In the ingravescent type of 
apoplexy compression, even ligation of the carotids, has been practised. 

Otherwise, the treatment in the early days consists of good nurs- 
ing, rest in bed for ten days or two weeks, the prevention of bed 
sores, attention to the position of the paralyzed limbs which may be 
enveloped in cotton wool, catheterization if necessary, and after the 
first day or two a light, nutritious diet. Stimulants and heart tonics 
should be avoided, unless cardiovascular collapse develops. In addi- 
tion, after the lapse of ten days or two weeks, the paralyzed limbs should 
be rubbed for ten to fifteen minutes twice daily, to maintain nutrition 
and lessen contractures, and at the end of three or four weeks the 
faradic current may be applied — especially to the extensors and abduc- 
tors — which are likely to be soon overcome by the contracting flexors 
and adductors. Iodide of potassium is often given, in the hope that it 
tends to promote absorption of the clot. It is of value in syphilitic cases, 
and in the event of recent syphilis may be combined with mercury. 
In the course of time resort to surgical intervention, tendon cutting or 
transplantation, and nerve transplantation, may be advisable to overcome 
disabling contractures. 



CEREBRAL THROMBOSIS. 

(Cerebral Softening.) 

Etiology. — Thrombosis of the cerebral vessels occurs under conditions 
that favor clotting elsewhere — the chief of which are arteriosclerosis and 
a weak or slow circulation. It most commonly follows syphilitic end- 
arteritis, and occurs in middle and advanced life. It may develop within 
small or fair-sized aneurysmal dilatations of the cerebral vessels, and 
after partial or complete obstruction by a clot. It may occur during the 
course of, or following, infectious diseases, and in conditions of blood 
impoverishment favoring clotting. 

Pathology. — Thrombosis is most common in the middle cerebral 
artery (supplying the motor cortex as well as the corpus striatum) and 
in the basilar arteries. The lesions are those of thrombosis in general, 
followed by an area of infarction, which may be red (or hemorrhagic), 
but often is pale (or anemic). The softened and necrotic area becomes 
replaced by a scar, or a cyst ensues, and the fibers deprived of continuity 
with their nuclei, degenerate. 

Symptoms. — The symptoms vary with the mode of onset and the region 
of the brain involved. Even extensive softening may be found without 
noteworthy symptoms (involvement of so-called silent areas of the 
brain). In some cases the onset is sudden and quite like that of hemor- 
rhage. In many cases, however, the onset is gradual, and may be pre- 
ceded by certain prodromes attributable to temporary anemia of certain 
regions of the brain, such as temporary inability to think, speak, see, 
remember, or to move certain muscles (ptosis, strabismus, etc.); or 



CEREBRAL EMBOLISM 869 

numbness or tingling in an arm or a leg. Out of these there may develop 
gradually progressing paralysis of an arm, a leg, half of the face or the 
tongue, or a partial or complete hemiplegia (depending upon the part 
of the brain involved — small or large areas of the cerebral cortex or the 
internal capsule, etc.); and these may or may not be attended by loss of 
consciousness, which, if it does ensue, is gradual in development. Both 
the unconsciousness and the paralysis are likely to lessen considerably, 
since, although usually looked upon as end arteries, some considerable 
collateral circulation may become established; but a permanent, partial 
or complete hemiplegia is the rule, as in cerebral hemorrhage. Aphasia 
(page 840) may ensue in left-sided lesions. Thrombosis of the basilar 
artery and its branches gives rise to lesions similar to those of hemor- 
rhage into the pons (page 866). Thrombosis of the posterior cerebral 
artery gives rise to hemianopsia and sensory aphasia. 

Diagnosis. — The diagnostic data are mentioned in connection with 
those of hemorrhage (page 867). 

Prognosis. — The outlook in general is rather better than in hemorrhage, 
but the tendency to thrombosis is likely to remain, and mental deterio- 
ration, loss of memory, etc., are likely to ensue. 

Treatment. — The treatment comprises efforts to ward off an attack, 
the imminence of which is suggested by the prodromes mentioned; these 
consist of measures useful in arteriosclerosis (page 493) and syphilis (page 
190), and cardiac stimulants, such as alcohol, ammonia, ether, caffeine, 
strophanthus, nitroglycerin, and digitalis (in small doses, and cau- 
tiously). The treatment of the developed attack should consist of 
rest, with the head low, and the aforementioned cardiac stimulants. 
Care should be taken not to depress the circulation and thus favor 
additional clotting. The general hygienic management and the use of 
massage and electricity are as has been mentioned in connection with 
cerebral hemorrhage (page 867). 

CEREBRAL EMBOLISM. 

{Cerebral Softening.) 

Etiology. — Cerebral embolism occurs most commonly in cases of 
chronic recurring endocarditis of the mitral and aortic valves, and is 
therefore most common in young subjects, especially women. Occa- 
sionally it occurs in other conditions in which emboli gain access to the 
general circulation (clots from an aneurysm, atheromatous plaques, 
etc.); and in conditions of arterial pyemia, but since these emboli are 
infected, a brain abscess ensues. 

Pathology. — Emboli reach the brain more commonly by the left than 
by the right carotid artery, and the lesions therefore are usually left- 
sided. They consist of plugging of a vessel, usually a branch of the 
middle cerebral artery, and an area of softening analogous to that 
which follows thrombosis. More or less widespread thrombosis may 
follow the embolic plugging of the vessel. 



870 DIFFUSE AND FOCAL DISEASES OF THE BRAIN 

Symptoms. — The symptoms are sudden in onset, although they vary 
with the site of lodging of the embolus. Usually the common symptoms 
of cerebral hemorrhage develop, and the patient is soon found to be 
hemiplegic and aphasic. Convulsions may occur in case the cortex be 
involved. 

Diagnosis. — The diagnosis is to be based upon the occurrence of 
hemiplegia or other paralysis in a young subject with endocarditis or 
other disorder whence an embolus may be derived. The differential 
diagnosis is like that of hemorrhage (page 867). 

Prognosis. — The prognosis is rather better than in hemorrhage, but 
the likelihood of recurrence must be borne in mind if the initiating 
factor persists. 

Treatment. — The treatment is that of thrombosis (page 869) plus the 
treatment of the primary cardiac or other disorder. 



THROMBOSIS OF THE CEREBRAL SINUSES. 

Etiology. — Thrombosis of the cerebral sinuses may be primary or 
secondary. The primary cases, which are usually simple or non- 
infected, may result from anemic states (chlorosis and severe anemias 
in general) ; cachectic states, such as diarrhceal and other wasting dis- 
eases of children, and advanced carcinoma, Bright's disease, etc., in 
adults; and infections such as typhoid fever, tuberculosis, etc. The 
secondary cases, which are usually infected, result from extension of 
disease of contiguous structures, especially middle-ear disease, brain 
abscess, fracture of the skull and subsequent infection, and extension of 
suppurative processes outside the skull (erysipelas and other pyococcic 
infections). 

Symptoms. — Thrombosis of the lateral sinus (usually associated with 
middle-ear disease) gives rise to pain, tenderness, and oedema over the 
mastoid, fulness of the regional veins, often induration of the internal 
jugular vein from extension of the thrombosis, and the general evi- 
dences of septicopyemia (chills, fever, sweats, and polynuclear leuko- 
cytosis), and often delirium. 

Thrombosis of the longitudinal sinus (which occurs usually in anemic 
and cachectic states, after typhoid fever, etc.) may not cause any ob- 
trusive symptoms, the symptoms of the primary disease being predom- 
inant; but headache, mental dulness, convulsions, and various paralyses, 
depending upon the portion of the motor cortex involved, may ensue. 
In the absence of infection there are no general symptoms due to the 
thrombosis itself. 

Thrombosis of the cavernous sinus (which usually follows infections 
of the nasal or orbital cavity) may give rise to frontal or lateral 
headache, oedema of the orbital tissues, exophthalmos, conjunctival 
ecchymosis, ulceration of the cornea, papilloedema, paralysis of the 
ocular muscles, etc. 



ABSCESS OF THE BRAIN 871 

Treatment. — The treatment of the infective cases is surgical, and 
should not be delayed. The treatment of the anemic and cachectic 
cases is that of the primary disorder, and the use of the iodides, iron, 
quinine, strychnine, etc. 



ACUTE HEMORRHAGIC ENCEPHALITIS. 

(Acute Hemorrhagic Cortical Encephalitis; Inferior and Superior Polioencephalitis; 

Cerebellar Encephalitis.) 

Etiology. — Local or diffuse inflammation of the brain substance 
occurs under varying circumstances: (1) It may follow fractures of 
the skull. (2) It occurs, to a greater or less extent, in all cases of men- 
ingitis. (3) It may develop about foci of hemorrhage and softening 
(embolism and thrombosis). (4) It may follow acute infections, such 
as diphtheria, scarlatina, influenza, pneumonia, etc. (5) It has been 
attributed to alcoholism, ptomaine poisoning, lead poisoning, carbon 
monoxide poisoning, etc. (6) It may occur as an independent disorder, 
perhaps an acute infectious disease, involving the cortex or the nuclei oj 
cranial nerves. In this, the superior and inferior polioencephalitis of 
Wernicke, the lesions consist of acute hemorrhagic inflammation of the 
gray matter about the aqueduct of Sylvius; these have been described 
under ophthalmoplegia (page 851). In other cases the lesions may be 
confined to the motor cortex, the acute infantile cerebral palsy of Strum- 
pell; a similar condition may be found in adults. In other cases the 
inflammatory process may be limited to the area of distribution of a 
single arterial branch, or it may involve corresponding areas of both 
hemispheres; or it may be disseminated in the cerebrum and the cere- 
bellum. The lesions consist of foci of congestion, hemorrhage, and 
softening, involving especially the gray matter; in many respects the 
condition is the cerebral homologue of acute poliomyelitis. 

Symptoms. — The symptoms are often equivocal; often for a time 
they are those of a general infection only, with headache, delirium, 
coma, fever, etc., but to these, focal symptoms are commonly added, 
varying with the seat of the lesions. There may be paralysis of an arm 
or a leg or of any of the muscles supplied by the cranial nerves, aphasia, 
anesthesia, convulsions (cortical or Jacksonian in type), etc. Death 
may ensue within several weeks, or, the acute symptoms subsiding, the 
condition may become chronic and more or less mental deterioration 
(imbecility) may persist. 



ABSCESS OF THE BRAIN. 

(Acute Suppurative Encephalitis.) 

Etiology. — Abscess of the brain is most common in young male 
adolescents and adults. The causes are: (1) Traumatism of the head, 



872 DIFFUSE AND FOCAL DISEASES OF THE BRAIN 

usually fracture of the skull, and subsequent infection. (2) Extension 
of suppuration from adjacent structures, especially middle-ear disease, 
with involvement of the mastoid, nasal suppuration, and necrosis of the 
bones of the skull. (3) Transport of infection from distant regions, 
such as lung abscess, bronchiectasis, empyema, (4) General septico- 
pyemia. The infectious agents comprise staphylococci, streptococci, 
pneumococci, Bacillus pyocyaneus, Bacillus influenzae, Bacillus tuber- 
culosis, Nocardia, etc. 

Pathology. — There may be one or many abscesses. Usually there is only 
one, which varies in size from 2 to 20 or 30 cm. in diameter, and is most 
common in the temporosphenoidal lobe or the cerebellum (on account 
of the proximity of the bones of the ear); but it may be situated in the 
frontal, parietal, or occiptal lobe. The pus is often greenish and has a 
foul odor. In acute cases there is likely to be considerable congestion 
and oedema of the surrounding brain tissue; in chronic cases there may 
be a more or less well-defined area of limiting neuroglial tissue, or the 
surrounding brain tissue may be rather widely infiltrated with pus. 
The multiple abscesses are usually small, often, indeed, microscopic in 
size; larger ones may form from coalescence of smaller ones. 

Symptoms. — Corresponding with the mode of development of the 
abscess, the symptoms may come on acutely or insidiously. The acute 
cases usually follow a trauma or rapidly progressing middle-ear disease. 
The chief symptoms consist of general nervous phenomena, such as severe 
headache, vertigo, vomiting, delirium, mental dulness, stupor or coma, and 
often papilloedema and slow pulse; focal nervous symptoms depending 
upon the situation of the abscess (see cerebrospinal localization, page 83 1 ) ; 
and the systemic manifestations of septicopyemic states, such as chills, 
fever, sweats, and polynuclear leukocytosis. In the chronic cases the 
abscess may slowly attain considerable dimensions without occasioning 
symptoms — so-called latent stage, which is the more likely to be present 
if the abscess develops in one of the so-called silent areas. Symptoms, 
when they ensue, are like those just mentioned, but less severe; regres- 
sion and exacerbation of the symptoms may occur from time to time, 
and the exacerbations may be associated with convulsions. In cases of 
general septicopyemic or of local suppurative processes elsewhere, the 
general and local symptoms due to these may overshadow those due to 
the brain abscess — which may not be recognized. 

Diagnosis. — The diagnosis depends upon an etiological factor, the 
general and local evidence of disease of the brain, and the systemic signs 
of pyogenic infection. Biain tumor (page 874) and meningitis (page 
830) must be excluded. 

Prognosis. — Unless evacuated, the abscess causes death by destroying 
or compressing vital regions of the brain, or by provoking suppurative 
meningitis or general septicopyemia. 

Treatment. — The treatment is wholly surgical, and consists in evacua- 
tion and thorough drainage of the abscess. This should be promptly 
resorted to, and is often followed by recovery. 



TUMORS OF THE BRAIN 873 



TUMORS OF THE BRAIN. 

Etiology. — Tumors of the brain are more common in males than in 
females, and they occur at all ages, but, as a rule, before rather than 
after the fortieth year; they are comparatively common in young sub- 
jects and children. Some cases seem to follow traumatism to the head; 
but otherwise the etiological factors are those of tumors in general, and are 
as ill understood. 

Pathology. — Tumors of the brain may be primary or secondary, and 
benign or malignant, but the so-called benign tumors (the type of tumor 
benign in other parts of the body) becomes in the brain more or less malig- 
nant and leads to death, because of the implication of vital structures. 
The common tumors are sarcoma, glioma (gliosarcoma), endothelioma, 
carcinoma, and fibroma; but to these one must add the tubercle (solitary 
tubercle, tuberculoma), gumma, and cyst, since these formations, espe- 
cially tubercle and gumma, are very common in the brain, and there are 
essentially tumors in their growth and manifestations. The tubercle 
(the most common) is usually secondary to tuberculosis elsewhere; it is 
generally single, but may be multiple; it varies in size up to that of a 
walnut, or larger; it occurs especially in young subjects; and it develops, 
as a rule, from the meninges (associated meningitis), although it may 
be fdund within the brain substance — near the cortex, at the base, or in 
the cerebellum. The gumma is usually multiple; it develops, as a rule, 
from the meninges; it is found most commonly at the base of the brain 
or in the cortex, and comparatively rarely within the substance of the 
cerebrum or cerebellum. The endothelioma and fibroma develop from 
the meninges or nerve sheaths and compress the brain. The glioma 
(gliosarcoma) develops from the neuroglia and infiltrates the brain sub- 
stance. Other sarcomas, as well as carcinomas, may develop in any 
part of the brain as secondary metastatic nodules. Cysts may be par- 
asitic (rare) or simple (softening cysts), and occur anywhere in the brain. 
Rarer tumors comprise psammoma, cholesteatoma, lipoma, osteoma 
(from 'he skull), angioma, aneurysm, etc. 

Symptoms. — The symptoms vary with the variety, situation, and ra- 
pidity of growth of the tumor. Rarely, a tumor is found after death, 
in the absence of noteworthy symptoms during life; usually it has occu- 
pied one of the so-called "silent areas." In the great majority of cases, 
however, there are characteristic symptoms; of these, one group, the 
general symptoms, develop irrespective of the situation of the growth; 
another group, the focal symptoms, depend upon the situation of the 
tumor. The important general symptoms comprise headache, vertigo, 
vomiting, and papillcedema and optic atrophy. Headache is almost 
always present, and once developed rarely disappears, although it 
may vary in intensity from time to time. It may be dull and aching; 
or a sensation of fulness and compression; or it may be extremely severe 
and paroxysmal, especially at night (syphilis). Sometimes it is localized 



874 DIFFUSE AND FOCAL DISEASES OF THE BRAIN 

— which rarely is of diagnostic significance, although, if associated with 
local tenderness, it may suggest the situation of a gumma and local menin- 
gitis. The headache is variously due to increased intracranial pressure, 
stretching of the meninges, pressure upon and irritation of sensory nerves 
(especially the fifth), localized meningitis, etc. Vertigo is often an in- 
tractable symptom, sometimes occurring spontaneously, and often set up 
by changes in posture. It may occur in association with tumors of any 
part of the brain, but is most common in tumors of the base, or the cere- 
bellum. Vomiting is common; it has no relation to taking food; it is 
usually unattended with nausea, the contents of the stomach, as a rule, 
being suddenly violently ejected without antecedent warning; it may be 
induced by sudden movements of the head (which may also cause ver- 
tigo). It is most common in tumors of the base of the brain — beneath 
the tentorium (great increase in intracranial pressure). Papillcedema 
(choked disk) in many respects is the most important, and, with the 
other symptoms, the most trustworthy manifestation of brain tumor. 
It occurs in at least 90 per cent, of the cases, and is most common in 
tumors of the base of the brain and cerebellum; the condition is usually 
bilateral; in some cases it is more marked on the side of the lesion; in 
other cases on the other side. The rapidity of its progress is sometimes 
an evidence of the rapidity of growth of the tumor (perhaps, more cor- 
rectly, of the rapidity of increase of intracranial pressure); often there is 
associated neuroretinitis. Optic atrophy is the usual sequel. 

There are other more or less important general symptoms, such as 
general irritability, apathy, somnolence (sometimes insomnia), melan- 
cholia, even dementia or mania. General convulsions sometimes occur, 
and are of importance, since they may be mistaken for epilepsy, and 
thus lead to overlooking of the brain tumor, at least for some time. If 
well studied, they may reveal a definite, well-localized onset (Jacksonian 
or focal epilepsy), of value in localizing the tumor. Syncopal and apo- 
plectiform attacks sometimes occur; the latter may be due to hemor- 
rhage into the tumor. The pulse is usually slowed, and may be irregular; 
toward the end of life it may become rapid. The temperature may be 
normal or subnormal; occasionally there is fever (inflammatory lesions 
in the brain or meninges). Polyuria and glycosuria are sometimes 
observed (increased pressure or irritation of the medulla); and the 
patient may emaciate. 

The focal or localizing signs of tumors of the brain are those men- 
tioned under cerebrospinal localization (page 831). 

Diagnosis. — The diagnosis may be based upon any two of the impor- 
tant general symptoms (headache, vertigo, vomiting, and papillcedema) 
and such localizing signs as may be detected by a careful examination. 
Since papillcedema may be present for some time and in notable degree, 
with little or no impairment of eyesight, the eyegrounds should be exam- 
ined in all cases in which the possibility of brain tumor exists. Brain 
abscess may be excluded by the absence of the etiological factors of 
abscess (local trauma, middle-ear disease, etc.), the less rapid progress 



HYDROCEPHALUS 875 

of the symptoms, and the absence of general evidences of infection 
(chills, fever, sweats, and polynuclear leukocytosis). Meningitis (page 
828), cerebral hemorrhage (page 862), cerebral softening (page 868), 
and sometimes uremia (page 759) must also be excluded. 

Prognosis. — The prognosis depends upon the nature and situation of 
the growth and its amenability to surgical removal. Gummas may be 
absorbed by antisyphilitic treatment. In other tumors the average 
duration of life is about two years or less. Death may occur suddenly, 
in an apoplectiform attack for instance, or during general convulsions, 
etc. 

Treatment. — The possibility always exists that the tumor may be syph- 
ilitic; and since less than 10 per cent, of the cases are at any time 
amenable to surgical removal, antisyphilitic treatment should be tried, 
especially in all cases of doubt. Preference should be given to in- 
unctions of mercury and the concurrent and subsequent use of the 
iodides in very large doses (150 to 250 grains, 5 to 8 grams, daily). It is 
useless to continue the treatment with mercury if no improvement occurs 
within four to six weeks. Marked improvement, even cure, has been 
reported from the long-continued use of the iodides, even in supposedly 
non-syphilitic cases; at all events, the headache is thus often notably 
relieved. The vertigo and vomiting may be mitigated by the bromides. 
Convulsions call for morphine and atropine hypodermicly. 

Otherwise the treatment is surgical and has two objects in view — the 
removal of the growth and the relief of symptoms. The decision for 
surgical intervention should not be too long delayed, and the operation 
should be undertaken if the focal signs indicate accessibility of the 
tumor. In the event of inaccessibility, the operation known as decom- 
pression may be undertaken. It is designed to relieve intracranial 
pressure, by removing a portion of the skull, and it frequently results 
in lessening of the headache, vertigo, vomiting, and papillcedema. Some 
temporary relief of the increased intracranial pressure may also be 
effected by lumbar puncture. 

HYDROCEPHALUS. 

Hydrocephalus is a condition characterized by the accumulation of an 
increased, and often very large, amount of serous fluid within the ven- 
tricles of the brain. This condition is sometimes spoken of as internal 
hydrocephalus, to distinguish it from external hydrocephalus, a collection 
of fluid between the brain and the dura mater. This occurs in atrophy of 
the brain (hydrocephalus ex vacuo), in advanced life, and after hemor- 
rhages, softenings, etc. 

Internal hydrocephalus may be congenital or acquired. The con- 
genital cases may be observed at birth, when the enlarged head may 
interfere with parturition, or it may not become apparent until the child 
is some months or a year old. The condition may occur in several mem- 
bers of the same family. The real cause is not known, although it is 



876 DIFFUSE AND FOCAL DISEASES OF THE SPINAL CORD 

likely some vice of development or a foetal meningitis obstructing 
the foramen of Majendie and leading to the intraventricular accumu- 
lation of fluid. The acquired cases may result from an ependymitis 
with marked serous exudation, a condition which Quincke believes to be 
angioneurotic in nature (Quincke's angioneurotic hydrocephalus); or 
they may be due to inflammatory (meningitic) or pressure (tumor) 
obstruction of the passage from the third to the fourth ventricle or of 
the foramen of Majendie. 

In the congenital cases and those developing in early life the head may 
be slightly or enormously distended. The bones of the skull are sep- 
arated and the fontanelles widened; the forehead overhangs the face, 
the eyes are recessed, and the bones of the face seem small (only rela- 
tively small in comparison with those of the skull). The brain is en- 
larged, the ventricles more or less distended, and the cortex, as a rule, 
correspondingly atrophied. Although rarely considerable intellectual 
development occurs, the mentality, as a rule, is variously impaired up 
to complete idiocy. Death usually occurs in childhood, but the patient 
may reach adult life. The cases developing in adult life can scarcely 
be recognized with certainty; the hydrocephalus is usually only an inci- 
dent in the course of the disease to which it is due. 



DIFFUSE AND FOCAL DISEASES OF THE SPINAL CORD. 

VASCULAR DISORDERS OF THE SPINAL CORD. 

Hyperemia, anemia, and oedema of the spinal cord, speaking generally, 
occur under circumstances like those that occasion similar conditions 
in the brain (page 861 et seq.). They often exist without noteworthy 
clinical manifestations. The symptoms attributable to posterolateral 
or toxic combined sclerosis, which is rather common in grave anemias, 
are mentioned on pages 375 and 858. Embolism and thrombosis, and 
consequent softening of large areas (myelomalacia), are comparatively 
rare in the spinal cord; but thrombosis of fine bloodvessels is quite 
common in the arteriosclerosis of advancing life, and is found also in 
conditions of choreiform and athetoid movements, paralysis agitans, 
etc. Hemorrhage into the spinal membranes (hematorrachis) is 
mentioned on page 826. 

HEMORRHAGE INTO THE SPINAL CORD. 

(Hematomyelia; Intraspinal Hemorrhage.) 

Etiology. — Hemorrhage into the spinal cord may be due to traumatism 
(fracture-dislocation, acute flexion of the cervical vertebra? without frac- 
ture or dislocation), to severe convulsive diseases, such as tetanus, or it 
may occur into an area of the cord the seat of antecedent disease, such 
as tumor, myelitis, syringomyelia, etc. 



HEMORRHAGE INTO THE SPINAL CORD 877 

Pathology. — The hemorrhage may be very small (microscopic) and 
multiple, or single and very large, infiltrating a considerable length of 
the cord. Usually it occurs into the gray matter, which in consequence 
is most destroyed; but more or less laceration and secondary disorgani- 
zation of the white matter may also be found. 

Symptoms. — The symptoms depend upon the seat and extent of the 
hemorrhage. Usually there is sudden onset of paralysis, attended by 
more or less pain. The hemorrhage occurring high up (in the cervical 
region) may occasion paralysis of all four extremities, and may soon 
lead to death (involvement of the medulla). In other cases only the 
arms or the legs may be involved; in some cases there is a more or less 
outspoken and typical Brown-Sequard paralysis (page 838). If recovery 
ensues, there is more or less wasting of the muscles innervated by the 
cells in the anterior cornua (the usual seat of the hemorrhage) of the 
segment or segments involved; this is commonly more marked on one 
side of the body than on the other, and is associated with varying sensory 
disturbances — usually tactile hyperesthesia on the side of most marked 
paralysis, and impaired pain and temperature sensibility, with pre- 
served tactile sensibility, on the opposite side. In most cases there is also 
more or less spastic paralysis of one or both legs (more marked in one 
than in the other), since the hemorrhage usually involves the pyramidal 
tracts (upper motor neuron) primarily or secondarily. 

Diagnosis. — The diagnosis is comparatively easy in traumatic cases, 
and, in any event, if the symptoms are sudden in onset (which always 
suggests hemorrhage). Impaired pain- and temperature sensibility, 
with unimpaired tactile sensibility, suggests involvement of the gray 
matter (which is usually due to hemorrhage). The presence of ante- 
cedent disorders (tumor, myelitis, syringomyelia), to which the hemor- 
rhage may be secondary, must be determined by eliciting the signs 
significant of these conditions. 

Prognosis. — The outlook depends upon the seat and extent of the 
hemorrhage, and the presence or absence of associated lesions. In 
uncomplicated cases recovery usually ensues, but more or less per- 
manent paralysis and disability persists. 

Treatment. — The treatment consists of enforced rest; perhaps in the 
early days the application of an ice-bag to the spine (of questionable 
utility); and attention to the general hygienic conditions (feeding, pre- 
vention of bed sores, catheterization, enemas, etc.). Pain may require 
the use of morphine; general nervousness, the bromides, chloral, etc. 
Painful contractures of the muscles may be relieved by massage and 
warm applications. The iodides have been recommended to promote 
absorption of the clot. 

In traumatic cases radiographic examination may be resorted to to 
determine the nature of the lesion, and fixation apparatus may be 
applied if necessary to maintain a desirable position. The question of 
operation must be considered. It is always wise to postpone this until 
the shock has passed; and in some cases, even for a week or thereabouts, 



878 DIFFUSE AND FOCAL DISEASES OF THE SPINAL CORD 

to distinguish between symptoms due to compression or concussion and 
those due to permanent damage to the cord. In the event of total 
transverse destruction of the cord an operation is useless. But operation 
should not be too long delayed; beneficial results are much more likely 
to follow early rather than late operations. 



CAISSON DISEASE. 

(Driver's Paralysis; Compressed Air Disease; The " Bends.") 

Caisson disease is a form of paralysis characterized especially by para- 
plegia that develops in persons who have worked under increased 
atmospheric pressure, upon their return to the normal pressure of the 
earth's surface. 

Etiology. — While the disorder may develop in perfectly healthy men, 
it is much more common in those in poor health, from any cause; in 
alcoholic, cardiac, nephritic, and obese subjects; and in "green hands" 
rather than in those who have worked for some time under increased 
pressures. 

Pathology. — The conspicuous lesions consist of air emboli in the 
veins and capillaries of the spinal cord, and foci of hemorrhage and 
softening. The disease is commonly attributed to concentration and 
compression, in the tissues of the body, of the normal gases of the atmos- 
phere, caused by the abnormally great pressures within the caissons, 
etc., and to the sudden release of these compressed gases upon the subject 
passing rapidly from a high to a low atmospheric pressure. The condi- 
tion, therefore, is due to the sudden expansion of gases in soft tissues, 
the brain and the cord, contained within an unyielding bony framework. 
McWhorter, in fatal cases, found the right side of the heart filled with 
gas, of which 80 per cent, was nitrogen and 20 per cent, carbon dioxide; 
and he found no abnormal gases. 

Symptoms. — The symptoms consist of the sudden development, im- 
mediately or several hours after the subject leaves the caisson, of severe 
pain in the back and legs, so that he is unable to move, doubles up 
(the " bends"), and falls to the ground. The pain is in the muscles — 
which are also tender to palpation and on passive motion. Pain in the 
joints (knees, ankles, hips, elbows, etc.) also may be complained of, and 
add considerably to the patient's disability. In addition, headache, 
vertigo, tinnitus aurium, deafness, vomiting, and marked prostration 
often ensue; or apoplectiform attacks, with hemiplegia or monoplegia, 
and perhaps aphasia, may develop ; or a true paraplegia may supervene. 
Death may occur in coma. 

Diagnosis. — The disorder is readily recognized from the relationship 
of the symptoms and the etiological factors. 

Prognosis. — The prognosis is good in most cases. Recovery usually 
ensues within several days; but death, or more or less chronic invalidism 
may follow. 



MYELITIS 879 

Treatment. — The disease can be considerably lessened by careful 
physical examination of subjects presenting themselves for work in 
caissons, and rejecting only those in perfect physical health; and by 
gradual decompression — that is, the use of air locks or pneumatic 
cabinets, in which the pressure is gradually reduced, so that the workers 
are gradually brought from the greatly increased to the normal atmos- 
pheric pressure. The developed disease is best treated by recompres- 
sion — that is, subjecting the patient to increased atmospheric pressure 
and later gradually reducing it. Ergot in large doses has also been 
recommended. 

MYELITIS. 

Myelitis, or inflammation of the spinal cord, may be a diffuse or a 
circumscribed process; it may involve only the gray matter — a disorder 
discussed under poliomyelitis (page 270), and polioencephalitis (pages 
850 and 851); it may involve a narrow vertical area of both white 
and gray matter — transverse myelitis, or it may occur in scattered areas 
throughout the cord — disseminated myelitis. 

Etiology. — Acute myelitis may be a primary or secondary process, but 
in all cases it must be ascribed to the activity of infectious microorgan- 
isms (or their toxins), although an analogous condition of softening 
(myomalacia) may result from interference with the blood supply 
(thrombosis or embolism, or compression). In some cases myelitis 
seems to be in itself an acute infectious disease, but no specific organism 
has jet been discovered. In other cases it follows the more common 
infections, such as typhoid fever, smallpox, pneumonia, dysentery, pyo- 
coccic and gonococcic infections, syphilis, tonsillitis, etc., the organisms 
gaining access to the cord variously by way of the bloodvessels or the 
lymphatics. In other cases myelitis follows meningitis and neuritis, 
and tuberculosis or syphilis of the vertebras and spinal meninges. It is 
said also to follow exposure to cold and damp, traumatism to the ver- 
tebrae, etc. It is most common in male subjects before the fortieth year 
(susceptibility to the common exciting causes). 

Pathology. — The lesions at first consist of swelling, congestion, oedema, 
and softening of the cord, so that the gray and the white matter may 
be indistinguishable (especially in transverse lesions). Microscopicly 
there is vascular congestion, cellular and fluid exudation, minute hem- 
orrhages, swelling and degeneration of the axons and their myelin 
sheaths, and vascular and other degenerations of the ganglion cells of 
the gray matter. Soon the softened area may take on a yellowish color, 
due to fatty degeneration of the elements within the inflamed zone. 
Ultimately, if the patient survives, with absorption and disappearance 
of the degenerated tissues, the neuroglia undergoes hyperplastic, and 
later cicatricial, changes, so that the zone of inflammation and softening 
becomes replaced by scar tissue. In transverse lesions secondary 
degenerations ensue, beginning within twenty-four hours; so-called 



880 DIFFUSE AND FOCAL DISEASES OF THE SPINAL CORD 

descending degeneration in practically all the columns of the cord, but 
especially conspicuous in the crossed and direct pyramidal tract, and 
elsewhere in the anterior and lateral columns (association fibers); and 
ascending degeneration in the posterior columns of Goll and Burdach, 
the direct cerebellar tract, and the anterolateral ascending tract of 
Gowers. 

Symptoms. — The symptoms vary with the seat and character of the 
lesion. The onset may be abrupt (myomalacia from vascular occlusion 
or myelitis) or more insidious (usually myelitis). Some fever is usually 
present in the inflammatory cases. The symptoms in transverse lesions 
consist of those due directly to destruction of a part of the cord and of 
secondary manifestations due to blocking of impulses in the cord. The 
symptoms due directly to the lesion (destruction of the lower motor 
neuron) consist of loss of voluntary muscular control, flaccidity, and 
wasting, and the reactions of degeneration in the muscles innervated 
by the spinal segment or segments involved; loss of the deep reflexes 
represented in the destroyed portion of the cord (destruction of the reflex 
arc); and anesthesia and paresthesia in the area of peripheral distri- 
bution of the dorsal roots involved (destruction of the sensory neuron). 
The secondary symptoms, those due to blocking of motor and sensory 
impulses in the cord, consist of spastic paralysis of the muscles below 
the lesion (legs), with rigidity, and ultimate contractures and deformities, 
but no reactions of degeneration and no atrophy, aside from that which 
follows disuse (disorder of the upper motor neuron); increased knee- 
jerks, ankle clonus, and the Babinski sign; hyperesthesia or anesthesia 
(protopathic, epicritic, and deep sensibility) below the lesion; loss 
of control of the vesical and rectal sphincters; and vasomotor and 
trophic disturbances, especially coldness and cyanosis of the extremities, 
bed sores at points of pressure (sacrum, heels, etc.), thin, glossy skin, etc. 
Just at and above the segmental level of the lesion there is usually a zone 
of hyperesthesia (irritation of the dorsal roots), which, together with the 
upper limit of the area of anesthesia, form the best guide to the deter- 
mination of the level of the lesion (see Plate I, page 803). 

The symptoms of myelitis occur in varying combinations, due to 
variations in the lesions. The following may be distinguished: (1) 
Transverse thoracic myelitis, of which the symptoms are those just nar- 
rated. (2) Transverse lumbar myelitis, which differs only in the fact 
that the cells of the lower motor neurons innervating the legs are likely 
to be involved, so that instead of spasticity, flaccid paralysis, and atrophy 
of the muscles, with lost knee-jerks and the reactions of degeneration, 
ensue. (3) Transverse cervical myelitis, in which, in addition to the 
general symptoms mentioned, there is likely to be paralysis and wasting 
of the muscles of the hand (cervical enlargement), inequality of the 
pupils (disorder of the cervical sympathetic), hyperpyrexia, and death 
from respiratory failure (involvement of the cervical roots from which the 
phrenic nerve is derived). (4) Involvement of the conus medullaris is 
rare, but involvement may be recognized by paralysis of the vesical and 



MYELITIS 881 

rectal sphincters and of the levator ani muscles, and anesthesia and 
other sensory disturbances of the buttocks, perineum, and external 
genitalia. (5) Acute ascending myelitis or "paralysis (Landry's par- 
alysis). This is undoubtedly an acute infection of the spinal cord, 
sometimes of the spinal cord and peripheral nerves, and perhaps also 
the bulb. It is characterized by fever and associated constitutional 
disturbances, and by a rapidly ascending paralysis, which, beginning 
in the legs, soon involves the trunk, the arms, and the muscles inner- 
vated by the bulb (especially the muscles of respiration), so that death 
usually results within a few days from respiratory or heart failure, or 
paralysis of the muscles of deglutition. Occasionally a recovery is re- 
ported. There may be few, if any, sensory changes; the bladder and 
the rectum may not be notably involved; and consciousness is usually 
preserved to the end. The nature of the disease is not well understood; 
all cases apparently included in this category are not alike. In some 
cases the reverse order of the onset and progress of the paralysis is 
observed — a descending paralysis. (6) Disseminated myelitis. In this 
varying combinations of motor paralysis and sensory disturbances may 
occur simultaneously or in succession in the legs, trunk, and arms; only 
a few muscles of a limb may show atrophy and the reactions of degener- 
ation; and the disturbances of sensibility may be complete or incom- 
plete in different parts of the limb. 

Acute myelitis may lead to death within a few days or a few weeks, or, 
if the lesions are slight, the initial phenomena, the paralyses, may sub- 
side more or less and the patient pass into what is often called chronic 
myelitis (perhaps in some cases the symptoms develop so insidiously as 
to merit the term chronic from the beginning). There is spastic para- 
plegia, muscular rigidity, and consequent deformity of the legs, lessened 
or abolished sensibility, and loss of control over the vesical and rectal 
sphincters. 

Diagnosis. — The diagnosis should be readily made by attention to the 
aforementioned symptoms, and the exclusion of compression of the cord 
(page 882), ataxic paraplegia (page 858), subacute combined (toxic) 
degeneration of the cord (page 858), disseminated sclerosis (page 859), 
and meningitis (page 828). 

Prognosis. — The acute cases often soon lead to death; this is almost 
inevitable in transverse cervical myelitis. In other cases more or less 
improvement may ensue, but the patient usually becomes permanently 
incapacitated. Death may result from secondary infections, such as 
pneumonia, cystitis, proctitis, bed sores, etc. 

Treatment. — Rest in bed is essential, but the patient should be fre- 
quently moved from side to side and on his back, and the most pains- 
taking care must be exercised to prevent bed sores, cystitis, etc. The 
bladder must be regularly evacuated by catheterization, and the rec- 
tum by the use of laxatives and enemas. During the active stage of the 
disease good results have been claimed from the use of the salicylates, 
hexamethylenamin, and mercury (by inunction), even in non-syphilitic 
56 



882 DIFFUSE AND FOCAL DISEASES OF THE SPINAL CORD 

cases. Painful contractures of the muscles may be relieved by massage, 
hot applications, the bromides, etc. After the subsidence of the acute 
phenomena, strychnine, massage, electricity, warm baths, etc., are indi- 
cated, and orthopedic and other surgical interventions to prevent and 
correct defoimities. 



COMPRESSION OF THE SPINAL CORD. 

(Compression Myelitis.) 

Etiology. — Compression of the spinal cord may result from caries 
of the vertebrae (usually tuberculous, sometimes syphilitic), fracture- 
dislocation or tumor of the vertebrae, tumor or cyst of the spinal 
meninges, and aneurysm of the thoracic or abdominal aorta. 

Pathology.— In the case of fracture or dislocation the compression 
may occur suddenly, and is attended by varying degrees of crushing up 
to complete destruction of a segment or severance of the cord, with asso- 
ciated hemorrhage. In other cases the compression is slow, though 
usually progressive; the cord where compressed is smaller and paler 
than elsewhere, and reveals more or less secondary degeneration of its 
various tracts and replacement neuroglial fibrosis. Various grades 
of meningitis may be associated, especially in the tuberculous and 
syphilitic cases. 

Symptoms. — In the traumatic cases of sudden onset the symptoms vary 
with the grade of compression; they may be those of a total transverse 
lesion (page 837). In the cases of more insidious onset muscular twitch- 
ings and pains, radiating in the course of the nerves, may occur from irri- 
tation of the nerve roots. In the course of time various paralytic and 
sensory phenomena develop, varying with the seat of the compression; 
these in general are analogous to those mentioned in connection with 
myelitis (page 880) and chronic hypertrophic pachymeningitis (page 
828). 

Diagnosis. — The diagnosis depends upon the symptoms mentioned and 
the signs of the primary disorder causing the compression. Special 
attention should be directed to detecting the early stages of caries of the 
vertebrae, which, because of the undefined character of its symptoms, 
often passes unnoticed: persistent pain (lumbago, etc.), vertebral ten- 
derness, muscular rigidity along the spine, more or less immobility and 
difficulty in executing vertebral movements, etc., should not be over- 
looked. When kyphosis, skoliosis, etc., have developed, the diagnosis 
is self-apparent. 

Prognosis. — The prognosis depends upon the cause, degree, and dura- 
tion of the compression. 

Treatment. — The treatment is that of the primary cause. In tuber- 
culous caries marked benefit and cure may be effected by rest, various 
orthopedic apparatus, and the general treatment applicable in tuber- 
culosis; the extent of the improvement in the nervous symptoms will 



TUMORS OF THE SPINAL CORD 883 

depend upon the amount of permanent damage done to the cord. 
Syphilitic cases require antisyphilitic treatment. Cases due to fracture, 
dislocation, or tumor may be relieved by surgical measures (laminec- 
tomy, etc.). 

TUMORS OF THE SPINAL CORD. 

Etiology. — Tumors of the spinal cord are more common in males than 
in females, and they may occur at any age, although they are most com- 
mon in young adults. The etiological factors are those of tumors in 
general and are as ill understood. 

Pathology. — Tumors of the spinal cord may be primary or secondary, 
and benign (so-called) or malignant; and for practical purposes, as in 
the brain, gummas and large or solitary tubercles are included among 
the tumors of the spinal cord. These spinal-cord tumors may be 
divided into: (1) The medullary or intramedullary growths (those 
within the substance of the cord). These comprise not more than 20 to 
25 per cent, of spinal tumors; the most common are the gumma, the 
tuberculoma, and the glioma (gliosarcoma). They give rise to enlarge- 
ment and distortion of the cord at the seat of growth, and to various 
secondary degenerations of the tracts destroyed or compressed. The 
glioma may become the seat of secondary softening and cavity formation 
(see syringomyelia, page 884). (2) The extramedullary growths, which 
develop outside the cord — from the spinal membranes, intravertebral 
fibro-alveolar tissue, the vertebrse, the intervertebral cartilages, etc., and 
comprise endotheliomas, sarcomas, fibromas, lipomas, hydatid and other 
cysts, gummas, tubercles, and secondary carcinomas. These compress 
the cord and give rise to lesions analogous to those due to compression 
from other causes (page 882). Tumors in general may develop in any 
part of the cord; they are more common on the dorsal and lateral than 
on the ventral surface. 

Symptoms.- — Intramedullary tumors give rise to initial motor paralysis 
and sensory disturbances, varying with the seat of development. Occa- 
sionally there is an early localized muscular atrophy (destruction of the 
cells in the anterior cornua); and this may be combined with dissociated 
anesthesia. In other cases the symptoms are those of a unilateral 
lesion (Brown-Sequard paralysis, page 838); that is, chiefly motor 
paralysis on the side of and below the segmental level of the lesion, and 
anesthesia on the other side. The tumor may continue to grow and 
ultimately give rise to symptoms of a more or less complete transverse 
lesion (page 837). In other cases, in which the gray matter is espe- 
cially involved, the symptoms of more or less outspoken syringomyelia 
ensue. 

Extramedullary growths give rise to pain, due to compression of the 
dorsal roots; generally at first this is unilateral, and it radiates vari- 
ously, although in ''root distribution" depending upon the segmental 
level of the lesion. Irritation of the anterior roots may cause muscular 



884 DIFFUSE AND FOCAL DISEASES OF THE SPINAL CORD 

twitchings and rigidity. Subsequently, in consequence of compres- 
sion of the cord, various motor (paralytic) and sensory disturbances 
ensue. These at first may be of the Brown-Sequard type; later, when 
there is more or less complete transverse compression of the cord, the 
symptoms consist chiefly of paralysis and wasting of the muscles corre- 
sponding to the segmental level of the growth, and anesthesia corre- 
sponding to the dorsal roots compressed; spastic paralysis without 
wasting below the level of the lesion; and perhaps later more or less 
complete anesthesia below the lesion and loss of control over the vesical 
and rectal sphincters. 

Diagnosis.— -The diagnosis is often in doubt; but when present, pain 
radiating in a root distribution and progressive paralysis are almost con- 
clusive evidence of an extramedullary growth. In other cases localized 
muscular atrophy and associated anesthesia, with the later development 
of Brown-Sequard paralysis or paraplegia, indicate an intramedullary 
growth. In most cases, however, one must be content with the diagnosis 
of intraspinal tumor, and should determine the level of the growth by 
attention to the segmental distribution of the motor and sensory phe- 
nomena. One must exclude compression of the spinal cord from other 
causes (page 882). 

Prognosis. — The outlook is bad unless the growth be a gumma or 
amenable to surgical removal, which, of course, is impossible in intra- 
medullary growths. 

Treatment. — The treatment is wholly surgical, unless the growth be 
a gumma. In case of doubt, therefore, recourse should be had to a 
course of antisyphilitic treatment for four to six weeks. If improve- 
ment does not follow, operation should be undertaken; otherwise, the 
treatment is symptomatic. 



SYRINGOMYELIA. 

(Spinal Gliosis.) 

Syringomyelia is a condition characterized by neurogliomatous new- 
growth about the central canal, with subsequent cavity formation ex- 
tending a variable length throughout the spinal cord. It should be 
distinguished from hydromyelia or dilatation of the central canal, which 
may occur, usually in minor grade, as a congenital condition or in con- 
sequence of the pressure of tumors, etc. 

Etiology. — Syringomyelia occurs especially in early adult life, and in 
both sexes. The definite etiological factors are not known. 

Pathology. — The cavity formation is most common in the cervical and 
upper thoracic portion, although it may extend throughout more or less of 
the length of the cord; it varies much in shape, being usually more or less 
rounded, but it may extend into one or both dorsal cornua; it generally 
takes the place of the central canal, but it may develop about the central 
canal, which may be found compressed somewhere in the periphery. The 



SYRINGOMYELIA 885 

condition is commonly believed to be the result of primary proliferation 
of the neuroglial tissue with consecutive degeneration and cavity for- 
mation. Some observers attribute it to a congenital defect of develop- 
ment, with distention of the central canal (hydromyelia) and consequent 
proliferation of the surrounding neuroglia. Although this condition 
may occur, syringomyelia seems undoubtedly to be a primary neurogliosis; 
the epithelial lining of the cavity found in some cases is that of the 
original central canal. 

Symptoms. — The symptoms are of slow and insidious onset and pro- 
gression; they vary with the position, size, and direction of the neu- 
rogliosis and cavity formation; and they result from destruction of the 
spinal-cord substance at different segmental levels, and from pressure 
upon adjacent tracts in the cord. Since the gray matter is primarily and 
most extensively involved, the following characteristic signs occur: (1) 
Dissociated anesthesia — that is, loss of the pain and temperature (pro- 
topathic) sensibility, with good or complete preservation of tactile 
(epicritic) sensibility in any part of the body; (2) progressive muscular 
atrophy, with fibrillary twitchings, and ultimate reactions of degenera- 
tion, usually developing first and remaining most marked in the arms 
(destruction of the cells of the lower motor neuron); and (3) trophic 
and vasomotor disturbances of the skin, such as injuries and burns not 
felt (loss of pain sense), local hyperemias and anemias, excessive sweating 
or dryness, localized atrophy, bullae, painless whitlows and abscesses, 
gangrene, perforating ulcers, etc. ; and of the bones and joints, such as 
arthropathies (considerable effusion into the joint, thickening of all the 
joint tissues, with final absorption of the bone and atrophy of the articu- 
lating surfaces); these resemble the similar arthropathies of tabes dor- 
salis, but are more common in the shoulder, elbow, and wrist than in the 
knee or ankle. Spontaneous painless fractures also may occur (due to 
brittleness of the bone). In addition, there may be more or less spastic 
paraplegia (involvement of the pyramidal tracts), or the manifestations 
of more or less complete transverse myelitis (page 880), depending upon 
the extent of the horizontal involvement of the cord. Often there are 
symptoms of unilateral (or perhaps bilateral) paralysis of the cervical 
sympathetic nerves (page 824), from involvement of the first thoracic 
segment (spinal centre for the cervical sympathetic). Extension of the 
lesions to the medulla may give rise to atrophy and fibrillary twitchings of 
the muscles of the tongue and face (usually, at first at least, unilateral), 
dissociated anesthesia of the face and head, oculomotor paralysis and 
nystagmus; and difficulty in speaking, swallowing, and breathing, and 
cardiac arrhythmia (so-called syringobulbia). Progression of the lesions 
to the sacral cord may result in loss of control over the vesical and 
rectal sphincters. 

Morvan's disease, a condition characterized by painless whitlows and 
other trophic or nutritional disorders of the hands, such as ulcerations, 
necroses, falling of the nails, etc., is now believed to be a variety of 
syringomyelia. The cases studied of recent years reveal also muscular 



886 NERVOUS DISEASES OF FUNCTIONAL NATURE 

atrophy and dissociated anesthesia, as well as cavitation of the spinal 
cord (when studied after death). 

Diagnosis. — The disease may be overlooked in the early stages, unless 
the dissociated anesthesia is carefully sought for; but this, the pro- 
gressive muscular atrophy, and the trophic disorders make the diag- 
nosis easy. 

Prognosis. — The disorder, as a rule, is slowly progressive, but it may 
last many years, and sometimes comes to a standstill; it is not in itself 
dangerous to life unless the medulla becomes involved. 

Treatment. — The treatment is purely symptomatic — massage and 
electricity to keep up the nutrition of the muscle, and perhaps strychnine 
as a general tonic. 



NERVOUS DISEASES OF FUNCTIONAL OR 
UNKNOWN NATURE. 



MIGRAINE. 

{Hemicrania; Sick Headache; Bilious Headache.) 

Migraine is a disorder characterized by paroxysmal attacks of severe 
headache, nausea, vomiting, and prostration, and usually preceded by 
certain visual disturbances. 

Etiology. — Migraine is much more common in women than in men; 
it occurs in neurotic subjects; and it sometimes, but not always, exhibits 
hereditary or familial tendencies. In the great majority of cases it is 
a reflex manifestation of disease of some organ of the body, and is 
found especially related to errors of refraction, disease of the naso- 
pharynx, of the female genitalia (especially dysmenorrhcea), and of the 
gastro-intestinal tract; in some cases it seems to be autotoxic and a 
manifestation of gastro-intestinal auto-intoxication, gout, uremia, etc.; 
it is perhaps sometimes vasomotor in origin — vasoconstriction followed 
by vasodilatation of the cerebral vessels and headache (suggested also by 
a primary facial pallor and blueness and coldness of the extremities and 
secondary flushing and perhaps sweating); it may replace an epileptic 
attack; in some cases no adequate cause can be assigned. The attacks 
may be induced by excessive and prolonged eyestrain (week-ends in 
school children and other students), by general fatigue, dietetic indis- 
cretions, constipation, menstruation, emotional excitement, etc. 

Symptoms. — In the majority of cases there are certain premonitory 
symptoms (for hours, a day, or more) that enable the patient to foretell 
the advent of an attack; these are especially visual — flashes of light, 
colored spectra, dimness of vision, etc.; or the patient may feel generally 



MIGRAINE 887 

dull, "headachy," and somnolent. The onset may be sudden, or there 
may be a more gradual increment of the premonitory headache; at all 
events, the headache becomes severe, and although usually limited to one 
side or temple (hemicrania), it may be bilateral and general. It is in- 
creased by auditory, visual, and sensory impressions of all kinds. In 
an hour or thereabouts nausea and vomiting supervene; retching may 
be marked, and, with the headache, leads to marked prostration. In 
the course of a short time the patient usually falls asleep, and awakes 
several hours later much refreshed, if not entirely well; in some cases, 
however, the attack may last two or three days. Various sensory 
phenomena are sometimes associated, such as numbness and tingling or 
anesthesia of the limbs; sometimes transient muscular weakness, or 
vertigo, tinnitus aurium, deafness, aphasia, etc. The attacks may occur 
at long or short intervals, and may continue throughout life. In women 
they may cease about the time of the menopause, and at about the age 
of fifty years in men. 

Diagnosis. — Although migraine is typically paroxysmal and unilateral, 
and attended by visual and other sensory disturbances, and nausea and 
vomiting, all attacks are not typical; other causes of headache, there- 
fore, must be inquired into — all possible sources of reflex irritation; 
diseases of metabolism, of the blood, of the cardiovascular system, of 
the urinary system, and of the brain and its membranes and the skull. 
In neuralgia there are paroxysms of pain, radiating in the area of dis- 
tribution of a nerve, and tender spots along the course of the nerve; and 
the visual signs and the nausea and vomiting of migraine do not occur. 

Prognosis. — The prognosis is the better the earlier the patient is thor- 
oughly studied and all possible sources of reflex irritation eliminated. 
The outlook is bad for cure in cases of long standing, but in even the 
most intractable cases much relief can be afforded the patient. 

Treatment. — The most essential part of the treatment is to prevent the 
attacks. In the great majoiity of cases this can be done by the proper 
correction of errors of refraction — even slight errors; in other cases, 
other sources of reflex irritation must be sought and adequately treated; 
the diet should be regulated (purin-free diet), the bowels opened thor- 
oughly daily, a hygienic mode of life insisted upon, and all factors that 
in any way tend in the individual patient to provoke an attack corrected. 
Bromides, salicylates, sodium benzoate, and potassium acetate (and other 
alkalies) also are serviceable in preventing attacks; as are also the saline 
cathartics taken daily before breakfast. During the attack the patient 
should go to bed in a quiet, darkened room, and abstain from food. If 
retching continues, it may be best relieved by lavage; local hot applica- 
tions, bismuth, cerium oxalate, cocaine, etc., may also be tried. The 
bowels should be opened by calomel or blue mass and a saline cathartic. 
Acetphenetidin, acetanilide, and similar drugs are often necessary for the 
headache; or one may give caffeine, sodium benzoate, or nitroglycerin 
(in the event of high blood pressure), or gelsemium or cannabis indica. 



888 NERVOUS DISEASES OF FUNCTIONAL NATURE 



EPILEPSY. 

Epilepsy is a disorder of the nervous system, characterized by recur- 
ring attacks of loss of consciousness, attended or not by convulsions. 
The attacks of momentary loss of consciousness unattended by convul- 
sions are know as petit mat, or slight attacks; those in which there is loss 
of consciousness and general convulsions are known as grand mat, or 
severe attacks; and those in which the convulsive seizures remain local- 
ized to a certain definite area or group of muscles, or at least always begin 
therein, and are often unattended by loss of consciousness, are known as 
Jacksonian epilepsy. 

Etiology. — In a majority of the cases epilepsy begins before puberty, 
and it involves the sexes equally. It rarely develops de novo after the 
twentieth year, the cases observed thereafter being usually either recur- 
rences of attacks occurring for the first time during childhood, or Jack- 
sonian epilepsy due to a local cortical lesion. In the so-called idiopathic 
epilepsy no definite cause can be assigned, although etiological impor- 
tance is attributed to certain hereditary influences, such as epilepsy, in- 
sanity, hysteria and other neurotic conditions, syphilis, and chronic 
alcoholism in one or both parents. In other cases the disease, or at least 
epileptiform convulsions, may be due to: (1) Injuries to the head re- 
ceived during birth, or vascular (hemorrhagic) disorders suffered soon 
thereafter and followed by persisting residual lesions (cerebral paralyses 
of infants and children). (2) Toxemias, such as infectious diseases (in 
infants and children), alcoholism (especially common in middle-aged and 
elderly chronic alcoholic subjects), plumbism, uremia, intestinal auto- 
intoxication (especially in infants and children). (3) Reflex factors, 
such as dentition, an adherent prepuce, intestinal worms, a foreign body 
in the auditory canal or the nose, errors of refraction, the irritation pro- 
duced by a cicatrix, onset of puberty, menstruation, etc. (4) Cardio- 
vascular disease, such as arteriosclerosis, which sometimes causes con- 
vulsive seizures in elderly subjects, and if associated with disorder of the 
bundle of His may lead to Adams-Stokes disease (page 420). (5) Organic 
disease of the brain, especially fracture of the skull and resulting irrita- 
tion of the brain by a spicule of bone, local meningitis, etc.; brain 
tumor; brain abscess; syphilis, etc. Many of these conditions can 
scarcely be classed as epilepsy in a true sense, although the convulsive 
seizure may be indistinguishable from that of true epilepsy; some of 
them are promptly cured by the removal of the exciting cause of the 
attack, such as a foreign body in the auditory canal, an adherent prepuce, 
a spicule of bone irritating the cerebral cortex, etc. ; but in some of these 
cases the "epileptic habit" may have become acquired, and the convul- 
sive seizures may not subside for some time. 

Pathology. — In the idiopathic cases there is no recognizable lesion. 
In the other cases there are the various lesions peculiar to the disorders 
mentioned. 



EPILEPSY 889 

The epileptic fit may be looked upon as a sudden discharge of nervous 
energy, provoked by influences which may be: (1) Toxic in nature, such 
as the poison of uremia; the products of perverted metabolism, such as 
ammonium carbamate, etc. ; (2) irritative, such as the various organic 
disorders of the brain mentioned; or (3) vascular; and these various 
toxic and other stimuli may, if sufficiently active, provoke the discharge 
of nervous energy (the convulsion) by acting upon normal nerve cells; 
but, as is likely more common, being not excessively active, they unduly 
stimulate subnormal or highly sensitive cells and provoke an altogether 
disproportionate discharge of nervous energy. 

Symptoms. — Grand Mal. — A typical attack of grand mal consists of 
an aura, a convulsive seizure with loss of consciousness, and certain after- 
effects. The attack apparently may originate in any part of the cerebral 
cortex, and the aura or premonitory sensations vary accordingly. These 
may be psychical in nature (a vague, dreamy, or terrified state) ; associ- 
ated with the special senses — visual (occiptal lobe), auditory (temporo- 
sphenoidal lobe), olfactory or gustatory; related to the abdomen and 
the viscera (sensations of epigastric " sinking" or distress, or palpitation 
or other sensations related to the heart — pneumogastric aura); or there 
may be a sensation of numbness or other paresthesia in a finger or a 
hand (sensory aura), or localized twitching (motor aura). These aurse 
may be absent; when present, they are usually of momentary duration 
— a few seconds to perhaps a minute or thereabouts. Very soon the 
patient emits a loud scream or yell (epileptic cry), falls to the ground 
without any conscious effort to protect himself from injury, and is imme- 
diately in a convulsive seizure and unconscious. The spasms, which may 
begin anywhere, soon become generalized, although not everywhere 
equally marked. At first they are tonic, and involving the muscles of 
respiration, lead to cyanosis and venous distention; in a few seconds they 
become clonic, intermittent, jerky, and often violent, provoking marked 
tossing about of the patient's limbs and body; the eyelids open and close, 
the eyes move about in varying directions, the face is intermittently dis- 
torted and relaxed, and the jaws open and close violently, in consequence 
of which the tongue is usually lacerated and blood-stained saliva issues 
from the mouth. The mine often and the feces sometimes are dis- 
charged involuntarily; and petechial hemorrhages may occur into the 
skin and conjunctivae. As a rule, in the course of one or two, rarely 
three or more, minutes the convulsive movements gradually cease and 
the patient, fully relaxed, falls into a profound coma. In some cases he 
can be more or less aroused after a short time, but he may sleep for hours 
and awake mentally confused and complaining of headache and muscular 
soreness; and there may be other after-effects, such as a trance-like state, 
loss of memory, aphasia, monoplegia, hemiplegia, mania, etc. — all of 
which soon subside, as a rule. Or he may become subject to post- 
epileptic automatism, and perform apparently purposeful acts, such as 
walking, riding, journeying, criminal acts, etc., without subsequent recol- 
lection thereof. In some cases the period of sleep is very short — rarely 



890 NERVOUS DISEASES OF FUNCTIONAL NATURE 

perhaps absent — so that soon after even a rather severe convulsion the 
patient may return to his former occupation. Attacks may occur once or 
more frequently daily, or at longer intervals — weeks, months, years. In 
some cases a number of convulsive seizures follow in rapid succession, 
the patient meanwhile remaining entirely unconscious; this, so-called status 
epilepticus, may continue for hours or a day or more; it is often attended 
by fever and rapid pulse, and may soon lead to death from exhaustion. 

Petit Mal. — Attacks of petit mat consist of momentary loss of con- 
sciousness, perhaps also vertigo and faintness, but no convulsions. 
The patient may suddenly stop talking or perfoiming some act, drop 
what he may hold in his hand, or take up some new act, and almost 
immediately revert to his former activity. The attack may pass almost, 
if not quite, unnoticed by the patient's associates, or they may observe a 
transient pallor of the face or twitching of a muscle. In other cases the 
patient may experience only the aura of the more severe grand mal. 
These slight attacks may occur alone at long or short intervals, or they 
may alternate with severe seizures. 

Jacksonian (Cortical, Partial) Epilepsy. — Jacksonian epilepsy is 
characterized by convulsive seizures that begin and usually remain 
localized in a certain definite group of muscles, and are often unattended 
by loss of consciousness; but in some cases the convulsions become more 
widespread, and consciousness may finally become lost. A study of the 
beginning of the convulsive seizures, commonly in the finger, hand, toe, 
or face, may lead to an accurate localization of the lesion, which is com- 
monly an irritative lesion of the motor or sensory cortex. 

Diagnosis. — Grand mal is usually readily recognized by the aura, the 
epileptic cry, the sudden loss of consciousness, tonic and later clonic 
spasms, laceration of the tongue, involuntary voiding of the urine, the 
postconvulsive sleep, and other after-effects. Attacks often occur at 
night, and, if unobserved by others, may be recognized by the involun- 
tary voiding of urine, laceration of the tongue, and a rather common 
mental confusion and headache in the morning. Hysterical attacks may 
be distinguished by associated emotional disturbances and hysterical 
stigmas; usually a gradual onset and rarely an injury when falling; crying, 
talking, or screaming during the attack; absence of complete uncon- 
sciousness, and of lacerations of the tongue and voiding the urine 
during the attack; longer duration of the attack, and the frequent 
possibility of stopping it by procedures such as throwing water in the 
patient's face, etc. Attacks of petit mal may be distinguished from vertigo 
due to other causes and syncope by the occurrence of actual, although 
momentary, loss of consciousness, and the absence of the ordinary causes 
of vertigo and syncope (heart disease, Meniere's disease, etc.). Jack- 
sonian epilepsy is in itself characteristic. The epileptiform convulsions 
due to other mentioned etiological factors should be recognized by deter- 
mining the presence of those causes in the individual case. 

Prognosis. — The prognosis varies, and depends upon the age when the 
disease developed, its severity, and the possibility of removing exciting 



EPILEPSY 891 

causes of the attack. In a considerable proportion of the cases cessation 
of the attacks or cure can be effected, but a tendency sometimes per- 
sists for the attacks to recur in later life. The prognosis is poor in the 
cases beginning in children and after the thirty-fifth year (many syph- 
ilitic); it is relatively good in those developing about puberty. In many 
cases, especially in cases of frequently recurring attacks, the mentality 
gradually becomes impaired. 

Treatment. — In all cases, upon the development of fits the most pains- 
taking care must be exercised to discover any possible source of irritation, 
since in the early stages removal of local irritations may lead to mitiga- 
tion if not cure of the disease. The best possible hygienic conditions 
must be secured. The child should not be forced to keep up in studies 
with others better endowed. Excellent results have been achieved at 
epileptic colonies where the patients are taught some interesting and use- 
ful manual occupation. The diet should be light, nutritious, and non- 
stimulating; recent studies suggest the wisdom of reducing foods con- 
taining purin bodies (meat, fish, tea, coffee, etc.), and some observers 
believe in the desirability of reducing the sodium chloride intake. The 
bowels should be opened regularly and thoroughly; colonic flushings 
seem sometimes to be of service (lessening intestinal auto-intoxication?). 

The epileptic seizure requires no special treatment, aside from care to 
prevent the patient's injuring himself; a mouth gag or similar contrivance 
between the teeth to prevent his biting his tongue (usually impossible, 
on account of the brevity of the attack); and loosening the clothing to 
facilitate breathing. 

On the whole the best medicinal treatment still seems to consist of the 
use of the bromides, despite some opinions to the contrary. Any of the 
bromides may be given, although perhaps the mixed bromides secure the 
best results. They may be combined with antipyrin (5 grains, 0.3 gram, 
thrice daily — H. C. Wood); or, to counteract the tendency to produce 
acne, they may be given as follows : 



1$ — Potassium bromide 4 drams 16 

Sodium bromide, 

Ammonium bromide, of each 2 drams 8 

Solution of potassium arsenite 45 minims 3 

Camphor water, sufficient to make 8 ounces 250 

S. — Two teaspoonfuls (10 c.c.) in water three times daily. 





0— M. 



Strontium bromide also may be used; and the dose of the bromides in 
general may be varied to suit the individual patient; more than 40 to 50 
grains (2.5 to 3.25 grams) daily is rarely required. The cases not bene- 
fited by these doses are not likely to be benefited by larger doses, and 
large doses not only produce acne, but almost certainly cause mental 
depression (bromism), and sometimes ultimate mental deterioration. 
Belladonna, atropine, sodium borate, nitroglycerin, thyroid extract, and 
other drugs, alone or in combination with the bromides, have also been 
recommended. In status epilepticus the bromides, chloral, morphine, 
hyoscine, etc., are indicated, and stimulants if the patient goes into 



892 Nervous diseases of functional nature 

collapse. In Jacksonian epilepsy operation is often of the greatest utility; 
it should be undertaken if the focal symptoms are definite and referable 
to an accessible region of the brain, especially if there is a history of 
injury to, or a depression of, the skull. 



HYSTERIA. 

Hysteria is one of the so-called functional disorders of the nervous sys- 
tem, consisting of a permanent abnormal psychic state (hysterical tem- 
perament), abnormal suggestibility, and divers transient motor, sensory, 
vasomotor, trophic, and other neurotic phenomena. 

Etiology. — Hysteria is very common in females, but it occurs also in 
males — more commonly than is generally supposed — and it is not un- 
common in children. Its manifestations may become obtrusive at any 
age, but they are most common at or soon after puberty or in early adult 
life. Heredity — hysteria, epilepsy, insanity, neurotic instability, etc., in 
one or both parents — is of predisposing influence; almost equally impor- 
tant is bad early training and education. The exciting causes of the 
initial manifestations comprise traumas, shocks of various kinds, emo- 
tional disturbances, etc. 

Pathology. — No definite lesions are known; the disease, therefore, is 
called functional, although doubtless there is some lesion which still 
eludes detection. Hysterical phenomena, of course, may accompany 
organic disorders. 

Symptoms. — The basis of hysteria is the permanent hysterical tempera- 
ment, which is said by Starr to be manifested " by an abnormally keen 
sensibility to all external impressions and sensations, by a high grade of 
imaginative power, by a susceptibility to suggestions, by an unusual 
desire for attention and notice, by variations in mood not due to apparent 
causes, by a lack of judgment, by a manifest incapacity to exercise con- 
trol over thought, emotion, and action, and by a tendency to act on sud- 
den impulses." 

The motor phenomena consist of convulsive attacks, paralyses, spasms, 
and tremors. The convulsive attacks (hysteria major), which are rather 
uncommon, bear some resemblance to epilepsy, which has suggested the 
term hystero-epilepsy — a misnomer. They are usually preceded by 
emotional disturbances, globus hystericus (a sensation of a lump or 
obstruction in the throat and consequent suffocation), etc. The onset 
is usually rather gradual, although it may be sudden; consciousness is 
not wholly lost; a tonic stage is followed by clonic movements and the 
adoption of various more or less grotesque attitudes. The attack often 
lasts upward of a half hour or more, and may be succeeded by a period of 
mental aberration — pseudomania, a dreamy state, lethargy, trance, etc. 
Incomplete or abortive attacks (hysteria minor) may occur; they are un- 
associated with convulsive seizures and may consist of attacks of causeless 
laughing and crying, grotesque attitudes, passionate attitudes (ecstasy), 



HYSTERIA 893 

catalepsy, somnambulism, etc. Hysterical paralysis may be mono- 
plegia hemiplegic, paraplegic (most common), or affect any or all the 
limbs variously, or only groups of muscles. The paralyses may come on 
slowly or suddenly and they may disappear as they came; they may be 
partial or complete, and they are often preceded by more or less muscular 
weakness (hysterical myasthenia). Some muscular atrophy may follow 
(from disuse), but there are no reactions of degeneration; the knee-jerk 
may be normal or exaggerated (never absent); an imperfect ankle clonus 
is said to be occasionally observed, but the Babinski sign is never elicited. 
The superficial reflexes may be abolished, especially when sensory 
changes are associated. Control over the vesical and rectal sphincters 
is maintained, but retention of the urine, with overflow, may occur. 
Partial or complete aphonia may ensue from paralysis of the laryngeal 
muscles, usually the adductors. In some cases of paraplegia the loss of 
power is apparent, not in the reclining or sitting posture, but only when 
the patient attempts to stand (astasia) or walk (abasia); in these cases 
there is usually no ataxia and no disturbances of sensation; most, if not 
all, of the cases are hysterical. There may be also involvement of the 
pharyngeal and other muscles supplied by the cranial nerves. Muscular 
spasms often occur; involving the arm, leg, or neck, they give rise to 
various contractures and deformities (which may relax during sleep or 
anesthetization); involving the muscles supplied by the cranial nerves, 
they may cause spasmodic ptosis, strabismus, deviation of the tongue, 
spasmodic oesophageal obstruction, etc. Sometimes peculiar dancing 
movements occur (a form of saltatory spasm). Tremors are very com- 
mon; they may be fine or coarse, rhythmic or arrhythmic, choreiform; 
and they may involve any part of the body, especially the eyelids, mouth, 
tongue, fingers, shoulders, legs, etc. 

The sensory phenomena consist of anesthesia, hyperesthesia, and 
paresthesia. Anesthesia is the most common; it is usually a hemi- 
anesthesia (skin and mucous membranes), which may be partial or 
complete for all types of sensibility, or the sensibility may be dissociated; 
in other cases it is limited to a distal portion of a limb (glove or stocking 
form), or a segment (cuff form); or it may occur in variously shaped 
patches, which may change from time to time. Hyperesthesia is a sig- 
nificant symptom, the basis of so-called hysterogenetic zones; these 
are most common over the ovaries, beneath the breasts, just below the 
ribs, and over the vertebrae (see Fig. 15, page 804). Pressure over these 
tender spots may induce hysterical "attacks," and promote their cessa- 
tion when they have developed. Paresthesic phenomena of various kinds 
(sensations of heat and cold, numbness, tingling, etc.) may be observed 
variously in different cases. Sensory phenomena referable to the special 
senses, especially the eyes and ears, are common and significant. The 
most important consists of concentric contraction of the field of vision, 
usually bilateral, but often more marked on the side of hemianesthesia 
(crossed amblyopia); perversion of color perception (dyschromatopsia), 
consisting usually of the recognition first of red or green, instead of the 



894 NERVOUS DISEASES OF FUNCTIONAL NATURE 

normal sequence of blue, yellow, red, green, and violet; sometimes all 
color perception is lost, everything appearing dull or grayish (achroma- 
topsia). Hysterical deafness may occur, and the sense of smell and of 
taste may be impaired or lost, usually only or more markedly on the 
side of hemianesthesia; and there may be also a nervous hysterical 
anorexia, vomiting, constipation, etc. 

Vasomotor and trophic phenomena are often observed in varying com- 
binations with the other phenomena; they consist of erythematous erup- 
tions, oedema, urticaria, dermographism, cutaneous gangrene (neurotic 
or hysterical dermatitis), etc. Fever (doubtless of artificial production) 
may be observed; and disorders of metabolism and of the secretions and 
excretions may occur. 

Diagnosis. — Hysteria may simulate almost, if not quite, all other ner- 
vous diseases; but, as a rule, it can be more or less readily distinguished, 
because the clinical picture is not typical of the simulated disease, and 
because, in addition, hysteria itself manifests certain characteristic phe- 
nomena. Hysterical phenomena are characterized by their frequent sud- 
den onset, variability from day to day, and frequent sudden cessation; 
by the character of the motor paralyses, and their association with the 
anesthetic and other so-called stigmas of hysteria; and by their occur- 
rence in a person of hysterical temperament. The differentiation of the 
attacks of major hysteria from epilepsy is mentioned on page 890. 

Prognosis. — The prognosis is good; many patients recover entirely 
spontaneously, and others under well-directed management. Many, 
however, may readily be made worse by a tactless physician; indeed, 
Babinski and other observers believe that almost, if not quite, the whole 
complex of hysteria (the motor, sensory, and other phenomena) results 
from suggestion to a susceptible subject by a maladroit or unskilful 
physician or other person : assuredly an extreme and not proved view. 

Treatment. — The treatment should consist in improvement in the gen- 
eral health, the eradication of any functional defects aside from the purely 
hysterical, good food, fresh air, etc. In addition, the hysterical tempera- 
ment and the abnormal suggestibility of the patient must be borne in 
mind — its potentialities for good as well as evil. The successful physician 
will exercise a firm, although tactful, control over the life and activities 
of the patient — for a time at least, regulating and commanding the daily 
life and diet of one; preventing introspection in another by enlisting her 
interest in some useful and absorbing occupation, charitable work, out- 
door exercise, etc. ; prescribing a modified, complete or incomplete Weir 
Mitchell rest cure in another, or a work cure in another, or a course of 
massage, electricity, or hydrotherapy. A resourceful psychotherapy 
finds here a special field of usefulness. In addition, tonics, such as iron 
and arsenic, and nervines, such as valerian and asafcetida, are useful 
from time to time. Hypnotism is rarely if ever indicated, and assuredly 
never in inexpert hands; it is a two-edged sword, and often cuts in the 
adverse direction. 



NEURASTHENIA AND PSYCHASTHENIA 895 

NEURASTHENIA AND PSYCHASTHENIA. 

(Nervous Debility or Disability; Nervous Exhaustion; Nervous Prostration.) 

Neurasthenia is a disorder of the nervous system, unassociated with 
demonstrable anatomical lesions, and manifested clinically by marked 
mental and bodily fatigue, which upon effort develop rapidly and dispro- 
portionately to the exciting cause; by undue irritability and response to 
external stimuli; and often by disturbances of the emotional and psychic 
functions. Psychasthenia nowadays is sometimes used as a synonym 
for neurasthenia, and it is sometimes restricted to that type of neuras- 
thenia in which the symptoms are mental rather than spinal. 

Etiology. — Neurasthenia may occur in men and in women. In a great 
majority of the cases there is a predisposing congenital factor — a ner- 
vous system ill adapted to the stress and stain (mental, physical, emo- 
tional) of modern life — well borne by the majority of mankind. One or 
both parents of neurasthenic or psychasthenic subjects are often found to 
have been neurasthenic, epileptic, hysterical, excessively emotional, alco- 
holic, insane, etc., and they transmit an unstable nervous system. De- 
termining factors of the nervous breakdown comprise overwork (physical 
and mental), worry, misdirected education, shocks, anxiety, insomnia, 
excessive alcoholism and venery ; infections, such as typhoid fever, syphilis, 
etc.; auto- intoxications, such as chronic gastric and intestinal derange- 
ments, gout, diabetes, nephritis, etc.; exogenous intoxications, such as 
ptomaine poisoning, plumbism, mercurial poisoning, etc.; disease of 
various organs of the body, such as the female genitalia, the kidney 
(nephroptosis), stomach (gastroptosis), eyes (eyestrain), etc.; prolonged 
residence in the tropics; and trauma. Most of these determining factors 
do not cause neurasthenia in the absence of the congenitally weak or 
unstable nervous system — the primary factor. 

Symptoms. — The symptoms differ in different cases, and they comprise 
a variable congeries of mental, motor, sensory, vasomotor, somatic, and 
sexual symptoms. The mental symptoms are almost always present and 
usually dominate the clinical picture (psychasthenia); they consist of 
general "nervousness," inability to concentrate the attention or to persist 
in mental effort, which of itself may induce headache, vertigo, and mental 
confusion; imperfect reception and retention of perceptions, and conse- 
quent loss memory; loss of confidence in one's ability, delay and dis- 
inclination in coming to conclusions, and impaired judgment; morbid 
fears (agoraphobia, cleithrophobia), and more or less compulsory 
ideas (which, however, verge upon, if they do not constitute, insanity); 
irritability of temper and exaggerated reaction to external impressions 
— of sensibility, sight (retinal hyperesthesia), hearing (auditory 
hyperesthesia), smell, etc.; and emotional disturbances. The eyes 
are readily tired by reading or other "close work" (refractive errors 
should be searched for) ; the visual fields may be contracted, or may be- 
come contracted under examination (fatigue contraction). The motor 



896 NERVOUS DISEASES OF FUNCTIONAL NATURE 

symptoms consist of muscular fatigue, readily induced and dispropor- 
tionate to the exertion; tremors, especially of the hands, and twitchings 
or habit spasms, especially of the face; and usually normal or exaggerated 
tendon reflexes, which readily become exhausted. The sensory symp- 
toms consist of a feeling of malaise, irregular, fugitive pains (in the head, 
the back, the legs, along the vertebrae), paresthesias (numbness, tingling, 
sensations of heat and cold), areas of hyperesthesia, especially about the 
head, along the vertebrae, etc. Vasomotor symptoms consist of readily 
induced pallor or flushing of the face, blueness and coldness of the 
extremities, excessive perspiration, dermographism, etc. The somatic 
symptoms comprise various symptoms referable to the heart (palpita- 
tion, vertigo, distressing pulsation of the arteries, etc.), of the gastro- 
intestinal tract (gastric neurasthenia, page 621), of the kidneys (lessening 
or increase in the amount of urine, phosphaturia), etc. The sexual symp- 
toms (sexual neurasthenia) comprise various paresthetic phenomena, 
nocturnal emissions, spermatorrhoea, imperfect erection, premature ejac- 
ulation, etc., in the male, and hyperesthetic and paresthetic phenomena 
unassociated with organic disease, frigidity, nocturnal involuntary or- 
ganisms, etc., in the female. The importance of these is often unduly 
exaggerated. 

Diagnosis. — The diagnosis rests upon the generally inherited neuro- 
pathic basis and the activity of some one of the many determining causes. 
But many organic diseases of the nervous system and of other organs 
may begin with "neurasthenic" symptoms, so that careful and repeated 
physical examination and prolonged observation may be required to 
exclude other disorders. 

Traumatic neurasthenia (the traumatic neuroses and psychoses) is a 
disorder of the nervous system that follow injuries and shocks, and is 
unassociated with gross lesions of the nervous system and the enclosing 
bony framework; it is often spoken of as "railway brain" and "railway 
spine." The condition is more common after accidenis in which the 
patient may not be notably injured, but suffers a "mental shock" in con- 
sequence of the suddenness of the accident or disquieting attending cir- 
cumstances (railway wrecks, etc.), than it is after accidents in which the 
patient may be more or less severely injured. The nature of the disorder 
is not known: it has been attributed to cerebral and spinal concussion; to 
organic lesions of the brain so slight as to elude detection; to disturb- 
ances in the intimate make-up of the cerebral cells; to psychic as distin- 
guished from cerebral disorder; and to malingering pure and simple. 
The symptoms in general do not differ from those of neurasthenia 
caused by other factors; only from the history of an injury can the phy- 
sician distinguish definitely the traumatic from the non-traumatic cases. 
The traumatic cases, however, as a rule, are rather more acute in onset, 
although they may not develop for days or weeks after the injury; mental 
symptoms are markedly in the foreground; hysterical manifestations are 
often associated, especially paralyses (monoplegic, hemiplegic, para- 
plegic) and anesthesias; and traumatic lumbago (due doubtless to 



OCCUPATION NEUROSES 897 

twisting or torsion- of the vertebras or stretching or laceration of the lum- 
bar muscle and ligaments) may also be present. The condition may last 
a long time, and may suddenly clear up entirely (sometimes very soon 
after the successful issue of a lawsuit); but mental deterioration, melan- 
cholia, etc., may ensue. 

Prognosis. — The prognosis should be guarded, since neurasthenia usu- 
ally occurs in a person with a more or less subnormal nervous system; the 
breakdown may be entirely recovered from, but the predisposition to 
a relapse is always present; so that, following recovery, the patient's 
life and work must be ordered well within his capabilities. 

Treatment. — As in the treatment of hysteria, so also in neurasthenia, 
success depends largely upon the physician, the confidence that he in- 
spires in the patient (psychotherapy), and the attention that he gives to 
detail. All possibilities of organic disease should be excluded by examina- 
tion and reexamination of the patient and assuring him that none exists; 
if found, it should, of course, be treated appropriately. All the func- 
tions of the body, the secretions and excretions, the diet, the daily life, 
must be regulated in accordance with the exigencies of each patient; 
and all the possible factors determining the breakdown must be 
carefully sought and rigidly excluded from activity. Errors of 
refraction should be corrected; a modified, partial, or complete Weir 
Mitchell rest cure is of much benefit in selected cases; others are better 
adapted to a work cure, a change of scene and occupation, a prolonged 
sea voyage, etc. Hydrotherapy is one of the best therapeutic measures 
at our command. Electricity may form part of the exaggerated psycho- 
therapy, the practice of which is now fashionable in certain quarters. 
The bromides for a short time are often serviceable, or one may use 
valerian, asafcetida, etc. Tonics, such as iron, quinine, mix vomica, 
arsenic, etc., are useful as occasion may demand. 

OCCUPATION NEUROSES. 

(Professional Neurosis; Occupation or Professional Cramps.) 

The occupation neuroses comprise a series of disorders characterized 
by cramps of muscles or groups of muscles concerned in the frequent or 
prolonged execution of certain voluntary coordinated movements. 

Etiology. — The occupation neuroses are more common in men than in 
women; most of the subjects are "neurotic/' endowed with a nervous 
system ill adapted to the prolonged strain to which it is subjected. The 
cramps occur most commonly in writers (writer's cramp or palsy), but 
also in telegraphers, typewriters, seamstresses, pianists, and others; the 
movements ultimately leading to the cramp may be fine and compli- 
cated (such as writing), or coarse and more or less simple. 

Pathology. — The nature of the disorder is not known; it has been 

variously ascribed to disorder of the muscles, the peripheral nerves, and 

the cerebral cortex; it is likely that much of the disorder emanates from 

the cells of the cerebral cortex, which perhaps become exhausted from 

57 



NERVOUS DISEASES OF FUNCTIONAL NATURE 

the necessarily prolonged effort to innervate the muscles; but whether 
this is the whole process is doubtful. 

Symptoms. — The symptoms consist of the development of spasms in 
groups of muscles concerned in the special cccupational activity; the 
spasms, as a rule, are tonic; occasionally there is a clonic or jerky move- 
ment. The spasms develop only when the special occupational activity 
is undertaken, the same muscles or group of muscles contracting nor- 
mally when acting independently or in other associations (in executing 
other movements). In writer's cramp there is a progressive disability; 
the movements of writing are performed with increasing effort and slow- 
ness; perhaps there is some associated tingling and aching in the muscles 
of the hand and the forearm, until finally writing becomes almost, if not 
quite, impossible from tonic spasm of the muscles; occasionally there 
may be a jerky clonic spasm (separation of the fingers, for instance), or 
tremors, or paresis. In a few cases some muscular atrophy, especially 
of the thenar, hypothenar, and interossei muscles, occurs (peripheral 
nerve disorder?). Similar phenomena, involving, however, other groups 
of muscles, occur in other circumstances, depending upon the occupation 
of the subject. 

Diagnosis. — The disorder is readily recognized from the occurrence of 
the spasms only upon the patient attempting certain special acts, and 
from the ability to perform other acts involving the same muscles. Neu- 
ritis may be excluded by the absence of pain and tenderness along the 
course of the nerves and of muscular atrophy. In the event of tremor, 
other disorders attended by tremor, especially multiple sclerosis, paralysis 
agitans, and progressive paresis of the insane, must be excluded. 

Prognosis. — Recovery may ensue if the patient discontinues the pro- 
voking occupation — at least for some time. 

Treatment. — The first essential is discontinuance of the special ac- 
tivities that provoke the spasms. The muscles involved should also be 
protected from such fatigue as may follow prolonged muscular movements 
of other sorts. Locally, hydrotherapy and massage are often serviceable; 
perhaps also galvanism. Attention should also be paid to improving the 
general health, as in neurasthenia. 

PARALYSIS AGITANS. 

(Shaking Palsy; Parkinson's Disease.) 

Paralysis agitans is a disease of the nervous system, unassociated with 
definite or constant anatomical lesions, and characterized clinically by 
muscular weakness, rigidity, and tremor, and a consequent characteristic 
facial expression, attitude, and gait. 

Etiology. — Paralysis agitans usually begins after middle life and is twice 
as common in men as in women. The onset is variously attributed to 
mental shock, worry, trauma, etc., but their real significance is undeter- 
minate. 

Pathology. — There are no definite or constant anatomical lesions. 
Changes have been found in the cortical nerve cells of the cerebrum; in the 



PARALYSIS AGITANS 899 

bloodvessels of the spinal cord (changes of an arteriosclerotic nature, and 
associated atrophic and sclerotic alterations in the gray and white matter 
of the cord); and in the muscles (especially in the muscle spindles). The 
disorder has been looked upon as a manifestation of senescence of the 
" nervous system; as a toxemia; as the result of some disturbance of the 
parathyroid bodies, etc. 

Symptoms. — The onset of the disease is insidious, although the first 
symptoms are sometimes referred to a shock or injury. The chief mani- 
festation consists of a slowly progressive weakness and rigidity of the 
muscles, usually (but not always at first) associated with tremors. The 
tremors, which develop in at least two-thirds of the cases, aie commonly 
first observed in 'the hands. In the beginning they may be slight and 
escape observation, but soon the forefinger and thumb (of one, but soon 
of both hands) are seen to be the seat of a so-called "pill-rolling" or 
"cigarette-rolling" movement; gradually all the fingers become in- 
volved; and ultimately the miiscles of the arm, leg, trunk, and face may 
share in the tremor. The tremors are fine (four to seven to the second) ; 
they are present during rest and quiescence; they are dimirTished, some- 
times abolished, at least temporarily, by voluntary movements; they usu- 
ally cease during sleep, and they are increased by excitement. The 
really characteristic manifestation of the disease is the muscular rigidity, 
which develops insidiously and becomes universal. It gives rise to the 
characteristic fixed and expressionless facial features (Parkinson's mask) ; 
to the dull and monotonous voice (rigidity of the muscles of the lips, 
tongue, and larynx); to a characteristic attitude — arching of the head 
and body forward (stooping posture), and flexion of the arms and hands 
(general overcoming of the extensors and adductors by the flexors and 
abductors); to the characteristic gait — steps at first slow and shuffling, 
but soon becoming short and rather rapid (festination), due to forward 
propulsion of the body and advance of, and the patient's effort to catch 
up with, his centre of gravity; in consequence of this the patient may 
ultimately fall forward; if suddenly started or pushed backward or 
laterally, a corresponding retropulsion or lateral pulsion may be 
observed. This muscular rigidity also results in delay in initiating 
voluntary movements, and in resistance to passive movements; mus- 
cular spasms also may occur. Muscular power is usually relatively well 
maintained for a considerable time. The tendon reflexes may be normal 
or exaggerated. Subjective sensations of heat, sometimes of cold, and 
dull aching in the legs or arms may be complained of, but objective sen- 
sory changes do not occur. Vasomotor disorders, such as a dry skin, 
sweating or flushing, and increased surface temperature, are occasionally 
observed. The patient is often apathetic, but when interested his men- 
tal faculties are usually found normal; he perhaps does not think as 
slowly as he must express himself. 

Diagnosis. — The disease is usually readily recognized; one must not 
overlook the cases without tremor. Multiple sclerosis is easily differ- 
entiated by the cessation of the tremor on voluntary movement (as 



900 NERVOUS DISEASES OF FUNCTIONAL NATURE 

contrasted with the volitional tremor), and by the other characteristic signs 
(page 859). With advancing age, but usually not much before the seven- 
tieth year, a fine tremor often develops (senile tremor) ; it usually involves 
the hands, and sometimes the neck and head (causing a slight nodding 
movement) and the legs; but it is not associated with the other signs of 
paralysis agitans. 

Prognosis. — The disease is incurable, although of itself it does not 
shorten life or lead directly to death. 

Treatment. — The treatment comprises a quiet life, freedom from worry 
and distress, and .the best hygienic and dietetic regimen. Hyoscine 
hydrobromate, duboisine, codeine and other preparations of opium, 
belladonna, cannabis indica, and extract of the parathyroid bodies have 
been recommended to control the tremors. Some benefit attends massage, 
hydrotherapy (hot baths), active and passive movements, and the use 
of tonics, such as arsenic, quinine, etc. 



ACUTE CHOREA. 

(Sydenham's Chorea; Chorea Minor; Infectious or Rheumatic Chorea; 
St. Vitus' Dance.) 

Acute chorea is a disease almost certainly infectious, involving chiefly 
the nervous system, and characterized clinically by involuntary, irregular, 
jerky muscular contractions and purposeless movements, and frequently 
associated with endocarditis and various psychic disturbances. 

Etiology. — Acute chorea is a disease of childhood, occurring especially 
between the fifth and the fifteenth year, and twice or thrice as commonly 
in girls as in boys. An inherited unstable nervous system (epilepsy, hys- 
teria, insanity, and other neuropathic taints in one or both parents) seems 
to be a predisposing factor. The exciting cause appears to be an infec- 
tious agent, as yet undiscovered, but allied to, if not identical with, that of 
rheumatic fever; a history of rheumatism may be elicited in from 25 to 
50 per cent, of cases of chorea, and cardiac murmurs are very commonly 
found clinically. Perhaps other infectious processes may be active etio- 
logically; but in some cases a history or evidence of infection cannot be 
obtained. Fright, shocks, and divers forms of reflex irritation (worms, 
errors of refraction, the harass of too strenuous education, etc.), are often 
put down as exciting causes, but their influence is unquestionably over- 
estimated. 

Pathology. — No constant or characteristic lesions have been described. 
The disease is rarely fatal; but congestion, swelling, and degeneration of 
the cerebral cortical cells have been reported, and Diplococcus rheu- 
maticus (Poynton and Payne) has been isolated from the meninges. The 
lesions of endocarditis are commonly associated. 

Symptoms. — The onset of the disease is, as a rule, gradual. During 
what may be called a prodromal period, of a week or more, the child 
may be listless, inattentive, generally nervous, restless, and unable to 



ACUTE CHOREA 901 

remain quiet. Soon, or in some cases, following a fright or emotional dis- 
turbance, the child is observed to be very nervous and to exhibit involun- 
tary, irregular, jerky, and purposeless movements. These may involve 
one or both arms (most commonly the fingers), or the legs, the face, one- 
half of the body, or the whole body; they vary much in degree from those 
that are slight and may almost pass unobserved, to those that preclude the 
possibility of the child's remaining still, and if involving the facial muscles, 
result in characteristic grotesque grimaces; they are increased by ex- 
citement, and may be augmented in the hands and arm, for instance, by 
getting the child to attempt to grasp some object (associated incoordi- 
nation); and they usually disappear during sleep. Involvement of the 
muscles of articulation results in defective speech, and sometimes various 
explosive (laryngeal) sounds; of the muscles of deglutition, in difficult 
swallowing; of the diaphragm and other muscles of respiration, in em- 
barrassed, irregular, or spasmodic breathing; and the cardiac action 
may become irregular. There is usually at least some muscular weak- 
ness; at times this may become marked in one or more limbs (paretic 
chorea). The tendon jerks, usually difficult to determine, are normal or 
slightly exaggerated. Cardiac murmurs and other evidences of acute 
endocarditis (usually mitral) are present in more than one-half of the 
cases, and often persist after recovery from the chorea; perhaps in some 
cases the murmur is due to incoordinated action of the papillary muscles 
rather than endocarditis. Other rheumatic manifestations, such as joint 
disorders, erythema nodosum, subcutaneous rheumatic (sometimes 
called fibrous) nodules, etc., may be present. The child, as a rule, 
is fretful and unruly; sometimes more marked psychic symptoms, such 
as mental dulness or depression, hallucinations, delirium, mania, etc., 
may occur. At the end of two to four weeks the more acute symptoms 
usually tend to subside, but the attack commonly lasts from one to three 
months, and recurrences are not uncommon. 

In some cases, however, the symptoms increase in intensity, or they 
may be very severe from the beginning — so-called malignant chorea 
(chorea insaniens). This is most common in early adult life and during 
pregnancy (toxic or infectious cases). The spasms are severe, general, 
and almost if not quite constant; they interfere with sleep and induce 
exhaustion; fever, delirium, and mania often ensue, and death usually 
results. 

Diagnosis. — The diagnosis, as a rule, is easy. One must differentiate 
habit chorea (habit spasm; one type of convulsive tic), a disorder of chil- 
dren, especially neurotic girls, which may or may not develop out of the 
frequent repetition of volitional acts (mimicry), and which consists of 
rapid coordinated acts, usually of a purposeful nature, and partly or com- 
pletely under the control of the patient's will. The movements are most 
commonly facial, such as winking, wrinkling the forehead, or drawing the 
mouth to one side, or they may consist of rapid shaking of the head, 
shrugging the shoulders, etc. The movements differ from those of acute 
chorea in their generally purposeful nature and in being confined to one 



902 NERVOUS DISEASES OF FUNCTIONAL NATURE 

muscle or group of muscles (frequent repetition of the same movement). 
One must also exclude the athetoid and choreiform movements of the 
cerebral paralysis of children (history of the case, permanent paralyses, 
arrested mental development, etc.); hysteria (more regular movements 
and other stigmas of hysteria); and paramyoclonus multiplex (shock- 
like, often symmetrical muscular movements, frequently involving the 
trunk). 

Prognosis. — The outlook is good, except in the so-called malignant 
cases. Recurrences, however, are common even in the mild cases. 

Treatment. — The child must be removed from school, all disturbing 
and exciting influences must be guarded against, and all possible sources 
of reflex irritation must be inquired into, and, if found, corrected. The 
best results follow confinement to bed for some time, or at least to the 
quietude of a sunny, pleasant room. The diet should be nutritious and 
not stimulating; coffee and tea must be prohibited. Hydrotherapeutic 
measures (warm baths, cold packs, etc.,) and massage are often of the 
greatest service. Arsenic (solution of potassium arsenite) is of distinct 
value in most cases; it should be given in doses of 2 to 3 minims (0.12 to 
0.2 c.c.) three times daily, and gradually increased to 6 to 10 minims 
(0.4 to 0.6 c.c); larger doses should be avoided. Salicyl preparations, 
belladonna, cimicifuga, and other drugs have been recommended. 
Quinine, bitter tonics, cod-liver oil, are often useful adjuvants. The 
severe cases require the use of sedatives, such as the bromides, chloral, 
chloretone, hyoscine, cannabis indica, valerian, etc. The cardiac com- 
plications are to be treated as are similar conditions developing under 
other circumstances. 



HEREDITARY CHOREA. 

(Huntington's Chorea; Chronic Progressive Chorea.) 

Huntington's chorea is a chronic hereditary disease of the nervous 
system characterized clinically by choreiform and ataxic movements, a 
staggering, ataxic gait, disorders of speech, and progressive mental deterio- 
ration. The disease bears no relationship whatever to acute (Syden- 
ham's) chorea. Its nature has not been definitely determined; in the 
few cases that have come to necropsy chronic meningo-encephalitis, with 
atrophy of the cerebral cortex, especially of the frontal and parietal con- 
volutions, has been found; in other cases, lesions analogous to hemor- 
rhagic pachymeningitis. Some observers postulate a congenital defect 
or maldevelopment of the nervous system. The disease begins usually 
in adult life, after the thirty-fifth year, occurs in succeeding generations, 
and affects several members of the family — the males more frequently 
than the females. The movements begin in the hands and feet and 
finally involve the entire body, including the trunk; they resemble those 
of acute chorea in being jerky and purposeless, but they are usually 
slower and more incoordinate (ataxic), and they are likely to be 



CONVULSIVE TICS 903 

bilaterally symmetrical. The gait becomes ataxic and staggering, some- 
times jerky; speech becomes slow and is sometimes varied by explosive 
sounds (involvement of the muscles of articulation). There is gradual 
mental deterioration, with loss of memory, delusions, etc., and final 
dementia. The disease lasts for years and is irremediable. It is readily 
recognized from its hereditary transmission, development in adult life, 
choreiform and ataxic movements, and progressive dementia. 

CONVULSIVE TICS. 

(Tic Convulsif; Impulsive Tic; Grilles de la Tourette's Disease.) 

The convulsive tics comprise a group of disorders characterized by 
the more or less frequent repetition of involuntary spasmodic muscular 
movements of a generally purposeful nature. These tics are of cortical 
origin, and represent, therefore, a psychosis; they are, in many respects, 
hysterical in nature, and may be associated with other hysterical phe- 
nomena; they occur in neuropathic subjects, and usually develop in 
childhood, although they may come on in later life. Sometimes they 
develop out of habit spasms (page 901) and mimicry; in some cases they 
are perhaps of reflex nature, having developed in consequence of errors 
of refraction (blinking), of disease of the nose, mouth, etc. The dis- 
order usually consists of involuntary, rapid, often lightning-like move- 
ments of the muscles of the face, such as blinking, wrinkling the fore- 
head, twitching about the mouth, etc. ; or there may be only fibrillary 
twitchings of certain muscles, such as of the eyelids (simple tics). In 
other cases the movements are more complicated, such as shrugging the 
shoulders, or convulsive movements of more or less of the body (complex 
tics). Sometimes the tics involving the laryngeal and associated muscles 
result in explosive cries or utterances; or words or names may be fre- 
quently repeated (echolalia), or obscene language used (coprolalia), or 
actions mimicked (echokinesis) — indicating the cortical nature of the 
disorder. A common psychic element in many cases is shown in the 
recurrence of a melody or harmony (mental equivalent of the muscular 
tic), in an almost irresistible impulse to touch objects (delire de toucher), 
to repeat words (onomatomania), to count before acting (arithmomania), 
in morbid fears (agoraphobia, cleithrophobia), doubts (folie de doute), 
etc. The disorder is usually readily recognized. In children it may be 
distinguished from chorea by the generally purposeful nature of the 
movements, their explosive, lightning-like character, their restriction to 
a group of muscles (the repetition of the same movement), the periods of 
freedom, and the associated psychic phenomena. Tic douloureux (page 
808) and other reflex tics are of an altogether different nature. The 
outlook is not especially good, although recovery may ensue, especially 
in children. In the treatment, special attention should be paid to all 
possible sources of irritation and to the general health. Benefit attends 
proper educational procedures and exercises, and attention to the under- 
lying neurotic condition. 



904 NERVOUS DISEASES OF FUNCTIONAL NATURE 



CHOREIFORM DISORDERS. 

Acute (Sydenham's) chorea, chronic hereditary (Huntington's) chorea, 
the habit spasms, the convulsive tics, and paramyoclonus multiplex are 
characterized by movements that more or less resemble one another and 
sometimes lead to diagnostic difficulties, but they should be readily dif- 
ferentiated, as already pointed out. In addition, there are the following 
choreiform affections* (1) Senile chorea, a disorder that occasionally 
develops in late middle life and much resembles Huntington's chorea, 
but differs in the absence of hereditary characteristics. (2) Dubini's 
electrical chorea, a rare disorder, characterized by rapid, violent, electric- 
like movements of the extremities, and sometimes also of the head and 
face; fever (perhaps infectious), ultimate atrophy of the muscles, and 
epileptiform convulsions are usually associated, and death supervenes 
after weeks or months. (3) Henoch's hysterical chorea, sl rare disorder of 
adults, characterized by sudden rhythmic electric-like contractions of 
the muscles of the shoulder girdle, of the neck, of the abdomen (Salaam 
convulsion), or of the psoas muscles, etc. It is likely hysterical in nature, 
and may be associated with other hysterical stigmas. (4) Saltatory 
spasm (latah, myriachit, jumpers), a disorder characterized by the occur- 
rence, when the subject attempts to stand, of strong contractions of the 
muscles of the legs and a consequent jumping or springing movement. * 
It is most common in neurotic men, and may occur endemically: in 
Maine and Canada (jumpers), in Russia (myriachit), in Java and its 
neighborhood (latah). 



FAMILY PERIODICAL PARALYSIS. 

Family periodical paralysis is a rare disorder that occurs in families, 
is transmitted from one generation to another, involves both sexes, and 
is characterized by paralysis of all the muscles supplied by the spinal 
nerves. The nature of the disease is not understood; it is believed to be 
toxic, since attacks may be induced by fatigue, constipation, infections, 
etc.; but they often come on without definite cause. Mitchell, Edsall, 
and others have found a lessened creatinin excretion for several days 
before the attacks, and a normal excretion after the attacks. The symp- 
toms develop rather insidiously, and consist of increasing lassitude and 
somnolence, and gradually progressing paralysis; this begins in the legs, 
and then involves the trunk and arms, and is usually complete at the end 
of twenty-four hours; the muscles innervated by the cranial nerves often 
escape entirely, but they may exhibit slight paresis. The paralysis is of 
the flaccid type; the tendon reflexes are lessened or lost; the superficial 
reflexes are diminished; and the electrical excitability of the nerves and 
muscles, especially to the faradic current, is diminished or lost. The 
heart may be dilated during the attack. Sensation and consciousness are 



HEAT STROKE 905 

unimpaired. At the end of twenty-four hours or thereabouts, the par- 
alysis begins to disappear, reversely compared to its development; re- 
covery may be complete at the end of forty-eight hours. The attacks 
may recur at irregular intervals — days, weeks, etc., and they may dis- 
appear permanently in advanced adult life. The prognosis is good, 
although rarely death has occurred during an attack. Potassium citrate 
has sometimes shortened or aborted an attack; otherwise the treatment 
is symptomatic. 

HEAT STROKE. 

(Sunstroke; Thermic Fever; Siriasis; Heat Exhaustion or Prostration; Insolations- 
Heat Cramps.) 

In consequence of exposure to excessive heat, one of three conditions 
may ensue — heat stroke, heat exhaustion, or heat cramps. 

Heat stroke (sunstroke, siriasis, thermic fever) is a condition that occurs 
after exposure to the sun's rays, and develops especially in persons who 
at the same time are engaged in hard manual work, such as railway and 
other laborers, soldiers on the march, etc. There are no constant or 
characteristic lesions; congestion of the brain, parenchymatous degen- 
eration of the solid viscera, undue fluidity of the blood, etc., have been 
found in fatal cases. The disorder is attributable to (toxic?) paralysis 
of the vasomotor centre in the medulla, provoked by the extreme or pro- 
longed heat; some observers look upon it as an infection. The onset 
of the disorder is sudden. There may be premonitory headache, vertigo, 
nausea, vomiting, malaise, etc., but often the subject suddenly drops to 
the ground, becomes unconscious, goes into deep coma, and soon dies 
from vasomotor paralysis and heart failure; or he may be found in 
deep coma, with high fever (108° to 111° F., or more), hot skin, flushed 
face, rapid pulse, labored, stertorous, or Cheyne-Stokes breathing, and 
complete muscular relaxation; occasionally fibrillary twitchings of the 
muscles or convulsions occur. Subcutaneous petechias may be found, 
the pupils are usually contracted (although at first they may be, and 
sometimes they continue to be, dilated). Death may ensue within twenty- 
four hours; or the temperature may fall, coma disappear, and recovery 
ensue. Often, however, the patient thereafter is unable to withstand the 
effects of high temperature; and occasionally mental deterioration, with 
loss of memory, etc., may ensue. 

Heat exhaustion, or prostration, is a condition that follows prolonged 
exposure to high temperatures (the sun's rays as well as indoor tempera- 
ture), and it occurs especially in those doing hard manual labor, such 
as workers in iron foundries, stokers in steamships (among whom poor- 
ventilation is doubtless a factor), soldiers on the march, etc. The 
condition is attributable to excessive sweating and insufficient water- 
drinking and consequent augmented specific gravity of the blood and 
inspissation of the tissues; a certain number of the cases, especially 
some, at least, of those occurring in the tropics, appear to be due in 



906 NERVOUS DISEASES OF FUNCTIONAL NATURE 

part at least to long-continued exposure to excessive light (the actinic 
rays of the sun), whence they may be termed "light exhaustion or 
prostration." The symptoms consist of initial headache, restlessness 
and vertigo; and profuse sweating, subnormal temperature (96° F. or 
less), muscular cramps, prostration, and collapse. The surface of the 
body is cool, as well as bathed in perspiration; the pulse is small and 
rapid, and the breathing rapid and shallow; consciousness, aside from 
its obscuration by the general prostration, may be maintained, but 
delirium may supervene (whence the not uncommon suicidal tendencies 
and sudden jumping into the water of stokers of ocean steam- 
ships). 

Heat cramps is a condition that develops in those who at the same 
time are exposed to great artificial heat and do much muscular work, 
especially workers in iron foundries, stokers on steamships, etc. It is 
described by Edsall as consisting of continuous fibrillary contractions 
of the muscles, especially those of the calves, and paroxysms of severe and 
painful, tonic spasms of the muscles, notably of the forearms and legs, 
but also of the abdomen, etc. The spasms occur spontaneously, and 
are provoked by efforts of voluntary movement and by mechanical, 
electrical, and other stimuli; and they last from one-half to one minute. 
An attack lasts, as a rule, not more than twenty-four hours, and is fol- 
lowed only by slight exhaustion and muscular soreness. Edsall attrib- 
utes the condition to an acute degenerative process in the muscles. 

Diagnosis. — The sudden onset of coma in those exposed to high tem- 
perature, and the high fever, serve, as a rule, to differentiate heat stroke 
from apoplexy and coma due to other causes; but one thus exposed, of 
course, may suffer an apoplexy or go into uremic or other coma, so that 
these must be excluded in all doubtful cases. Heat stroke, heat exhaus- 
tion, and heat cramps each is so distinctive that no difficulty should be 
experienced in differentiating them. 

Prognosis. — The outlook in heat stroke is good if the patient is brought 
promptly under treatment; but in some cases death ensues almost imme- 
diately, or within twenty-four hours. The prognosis in heat exhaustion 
and heat cramps is good. 

Treatment. — In heat stroke the bodily temperature should be reduced 
as promptly as possible — by cold-water or ice-water bathing, not forget- 
ting to apply cold to the head; cold- or ice- water enemas also may be 
employed. Venesection is valuable in markedly asphyxiated subjects, 
and chloroform in the event of continued convulsions. Stimulants, such 
as strychnine, camphor, ammonia, whiskey, etc., should be employed 
in case of marked prostration. These, as well as external heat, are 
necessary in heat exhaustion. Enteroclysis and hypodermoclysis, with 
physiological saline solution, are valuable in all toxic states, including the 
cases of heat exhaustion and heat cramps, in which there has been 
much sweating and comparatively little water drinking. Morphine or 
apomorphine may be resorted to if necessary to control the painful 
myospasms. 



ERYTHROMELALGIA 907 

VASOMOTOR AND TROPHIC DISORDERS. 



ANGIONEUROTIC (EDEMA. 

(Quincke's Disease.) 

Angioneurotic oedema is a disorder characterized by the occurrence 
of localized transient cedematous swellings of the skin and mucous mem- 
branes. It may be hereditary, and is believed by Quincke to be a vaso- 
motor neurosis leading to increased permeability of the bloodvessels. 
Some attacks seem to be precipitated by articles poisonous to the indi- 
vidual, such as shellfish, certain berries, etc.; by ptomaines; by gouty, 
gastro-intestinal, or other autotoxic states, etc. The face, the limbs, the 
trunk, may be the seat of these swellings, which cause local redness, dis- 
comfort, pain, and itching; in the mouth and pharynx they may impede 
swallowing; in the larynx they may cause dyspnoea, stridor, and more 
or less asphyxiation; and in the gastro-intestinal tract they may give rise 
to more or less severe colicky pain, nausea, vomiting, and diarrhoea. 
They may be associated with erythema, urticaria, purpura, etc. (page 389). 
The attack may last only a few hours, or a day or two, and it may recur 
at regular or irregular intervals. The treatment is not very satisfactory. 
The intestinal tract should be thoroughly cleared by means of blue mass 
or calomel and saline cathartics; inquiry should be made into all possible 
exciting causes, especially articles of diet (which may be toxic to the 
individual and not to others); and nervines, tonics, such as strychnine, 
and so-called intestinal antiseptics, may be prescribed. 



ERYTHROMELALGIA. 

(Red Neuralgia; Weir Mitchell's Disease.) 

Erythromelalgia is a disorder characterized by pain, tenderness, con- 
gestion, and increased temperature of the feet and sometimes of the 
hands, which develop especially when the parts are dependent. The 
disorder may apparently occur as an independent disorder — a so-called 
vasomotor neurosis; but similar phenomena may be associated with 
arteriosclerosis, multiple neuritis, etc. The symptoms begin with pain 
(usually burning in character) and tenderness in the feet, especially the 
soles; soon capillary distention supervenes and the feet become at first 
dusky red (often patchy, rather than uniformly); the arteries may pul- 
sate visibly, the veins become dilated, and the local temperature become 
increased; but after some time the foot becomes purplish red, or of a 
pallid cyanotic hue, and cold. The hands are occasionally involved. 
The phenomena are aggravated by the dependent position, exercise, and 
warmth; they may be induced in susceptible subjects by long standing. 



908 VASOMOTOR AND TROPHIC DISORDERS 

They may occur paroxysmally or become more or less permanent. A 
non-dependent position of the limbs, cool applications, massage, and 
electricity are of more or less avail, but the disease is usually quite in- 
tractable. 

ACROPARESTHESIA. 

Acroparesthesia is a painful disorder of the fingers and hands that 
occurs especially in women who do considerable washing (long immersion 
of the hands in hot water), and sometimes in men as well as women who 
use the hands a great deal. It is often associated with general ill health 
and impaired nutrition. It is perhaps sometimes of vasomotor origin, 
but it may also be neurotic, neuralgiform, or arteriosclerotic. The chief 
complaint is of numbness and tingling of the fingers and hand, which are 
likely to occur after prolonged immersion in hot water (therefore, toward 
night), or upon exposure to the heat of a fire, etc. Occasionally there is 
slight motor weakness and difficulty in executing fine movements (gen- 
eral involvement of the nerve). The symptoms vary in severity and 
duration. Usually they cease with cessation of the provoking cause, and 
they may be ameliorated by massage and electricity. 



RAYNAUD'S DISEASE. 

(Local Syncope; Local Asphyxia; Symmetrical Gangrene.) 

Raynaud's disease is a disorder characterized variously by symmet- 
rical syncope, asphyxia, or gangrene. In the early stage (local syncope) 
the fingers or toes, or both, and occasionally the ear tips or the nose, 
appear pale and cold — the so-called "dead" fingers and toes of the laity. 
This is analogous to the condition (chilblains) that may be produced by 
great cold (the low temperature of winter), and is attributed to spasm 
and incomplete obstruction of the peripheral arterioles. It may last for 
several hours or more and then subside, but in many cases a reaction 
ensues and the affected part becomes red or purplish, burning, tingling, 
and swollen (local asphyxia); sometimes exquisitely painful and more 
or less anesthetic. This is attributed to complete spasmodic obstruction 
of the arterioles and stagnation of the venous circulation; all fingers or 
toes may not become thus affected at once; one may remain pale and 
cold and its neighbor become cyanotic. In some cases the disorder con- 
sists of recurring attacks of such pallor and succeeding asphyxia of the 
fingers and toes; and the attacks may be set up by exposure to cold 
(worse, therefore, in winter), by emotional disturbances, by gastro- 
intestinal disorders (toxic ?), etc. In other cases the lesions progress to 
local gangrene and sphacelation of the finger- and toe-tips; rarely, to more 
extensive loss of tissue, or multiple foci of gangrene in other parts of the 
body. In some cases there has been a curious association of these 
phenomena of Raynaud's disease and paroxysmal hemoglobinemia 



RAYNAUD'S DISEASE 909 

(vasomotor disturbance in the kidneys ?) ; these have occurred together, 
and in other cases the hemoglobinemia apparently has replaced the attack 
of the more familiar phenomena. The cause of the arterial spasm is not 
definitely known: Raynaud believed it to be of central origin; others 
attribute it to reflex or toxic causes; and others look upon it as syphilitic 
or as a phenomenon of arteriosclerosis and thrombo-angiitis. The diag- 
nosis is readily made, and should exclude the cases due to manifest 
cardiac and arterial disease, ergotism, etc. The treatment should consist 
of a horizontal position of the limbs, wrapping the affected fingers 
and toes in cotton wool, and warm local applications. Nitroglycerin 
and other vasodilators, massage, and galvanism (the positive pole to 
the affected limb immersed in saline solution) are often of service. The 
pain may require the use of morphine or other narcotics and sedatives. 



SECTION XL 
DISEASES OF THE MUSCLES, 



MUSCULAR RHEUMATISM. 

{Myalgia.) 

Muscular rheumatism, or myalgia, is a disorder of the voluntary 
muscles and the related fasciae, characterized by pain which is markedly 
aggravated by motion. 

Etiology. — Muscular rheumatism is more common in men than in 
women; it occurs especially in those exposed to wet and damp, or di- 
rectly to a draught of cold air (open window, etc.) and sudden cooling, 
particularly after exercise sufficient to induce sweating. In many re- 
spects it is analogous etiologically to, and may be the muscular equivalent 
of, rheumatic fever; at all events, it occurs in "rheumatic" and "gouty" 
subjects. 

Pathology. — The nature of the disease is not definitely known. It is 
probably an inflammation of the fibrous investment of the muscular 
fibers and of the related fasciae and periosteal attachments of the muscles; 
but some observers look upon it as a disorder of the sensory nerve endings 
in the muscles. 

Symptoms. — The symptoms may come on suddenly or insidiously, and 
continue either a short or a long time (several hours to several weeks). 
The chief and often the only complaint is pain in and about a muscle 
or muscles; there is sometimes a little fever, but rarely any other general 
disturbance. The pain may be dull and aching, or sharp and cramp- 
like; it is markedly aggravated by any movement that involves the 
affected muscles, and it often, therefore, effectually prevents motion and 
leads to more or less contracture and malposition. Common types of 
the disorder are: (1) Lumbago, involvement of the lumbar muscles, 
which is usually very painful and often completely incapacitates the 
patient. One should exclude disease of the vertebrae, sacro-iliac joint, 
etc. (2) Pleurodynia, involvement of the intercostal muscles, and some- 
times the pectorals or the serratus magnus. It is usually very painful, 
on account of the necessary respiratory movements of the chest. There 
may be circumscribed tenderness over the involved and contracted 
muscles. Pleuritis can be excluded by the absence of friction sounds; 



912 DISEASES OF THE MUSCLES 

and intercostal neuraliga, by the absence of pain following the course of 
the nerves, of acute unprovoked exacerbations of pain, and of the painful 
or tender spots (page 809). (3) Torticollis (wry-neck), involvement of the 
sternomastoid muscle and sometimes of other regional muscles (back of 
the neck especially). The sternomastoid muscle stands out as a tense, 
painful, and tender cord, and causes rotation of the head and chin toward 
the unaffected side. 

Treatment. — In many cases prompt relief follows the use of remedies 
advised for rheumatic fever (page 256). In addition, rest to the disabled 
muscle or muscles is of the greatest importance. Pleurodynia is usually 
markedly benefited by strapping the side, or by a light application of the 
Paquelin cautery — which is also of the greatest service in lumbago. Hot 
applications, chloroform and other liniments, belladonna plasters, 
massage, galvanism, etc., afford relief in other cases. A hot or Turkish 
bath may cause almost immediate cessation of the pain. In obstinate 
chronic cases the iodides, mercury, belladonna, and iodine ointment, 
and attention to the dietary (antigout diet) are usually efficacious. 



MYOSITIS. 

Inflammation of the muscles is a rare disorder; but it may occur as a 
secondary, and apparently also as a primary, process. Secondary myo- 
sitis may be: (1) Suppurative, in which case it is usually part of a gen- 
eral pyococcic process (page 61)), with multiple muscular foci, although 
rarely perhaps there may be only a single muscular focus. The involved 
muscle is at first swollen and painful, and gradually goes on to abscess 
formation; the abscess, if not evacuated, may lead to or increase the 
general pyococcic process. (2) Syphilitic. Early in the infection there 
may be a cellular myositis; late gummatous formation may occur. The 
gumma being absorbed gives rise to more or less loss of muscular sub- 
stance and consecutive fibrosis. Primary myositis is very rare; occa- 
sionally it is observed as part of a dermatomyositis, a condition in which 
dermatitis and multiple involvement of the muscles and oedema occur. 
The muscles become tense, firm, and oedematous, and later degenerated 
and atrophic. In some cases hemorrhage may occur into the involved 
muscles (hemorrhagic polymyositis). The condition resembles trichi- 
nosis, but may be differentiated by the absence of eosinophilia and of the 
parasite in a piece of excised muscle. 



PROGRESSIVE MUSCULAR DYSTROPHY. 

(The Muscular Dystrophies; Primary Myopathy; Pseudohypertrophic Muscular 

Paralysis.) 

Progressive muscular dystrophy is a primary disorder of the muscles 
characterized clinically by progressive muscular wasting. 



PROGRESSIVE MUSCULAR DYSTROPHY 913 

Etiology. — Progressive muscular dystrophy is more common in males 
than in females. In most cases the disease is hereditary, being trans- 
mitted, as a rule, by the females to the males; in other cases it is familial, 
several members of the same generation being affected; some cases, how- 
ever, exhibit neither hereditary nor familial characteristics. Infections, 
injuries, shocks, etc., have been variously looked upon as exciting causes, 
but at most these are of only secondary significance, the predisposition, 
the primary myopathy, being present. 

Pathology. — The chief lesions consist of atrophy (which may be pre- 
ceded by hypertrophy) of the muscular fibers, replacement fibrosis, and 
the deposition in the connective tissue of fat. The process may progress 
to complete atrophy of the muscular fibers, although the muscle 
spindles are likely to remain intact, and the deposition of fat may be so 
marked as to cause notable enlargement of the part (pseudohypertrophy; 
hypertrophic lipomatosis; pseudohypertrophic muscular paralysis). The 
nervous system usually exhibits no lesions; rarely, degenerated changes 
have been seen in the cells of the anterior cornua of the spinal cord, and 
functional or other changes beyond our present means of detection have 
been postulated. The disorder appears to be unquestionably a primary 
myopathy — a muscular abiotrophy; the individual is born w T ith a muscular 
system ill adapted to the exigencies of life, so that sooner or later it 
begins to succumb and atrophy. 

Erb has classified the cases into (1) those that begin in infancy and 
childhood, and (2) those that develop in adolescence or early adult life 
(between which there is no essential difference); and he has also classi- 
fied them into (1) those in which there is a true hypertrophy of the mus- 
cular tissue, or a pseudohypertrophy (hypertrophic lipomatosis) of the 
part, and (2) those in which there is progressive atrophy of the muscle 
without the accumulation of fat ; but between these cases there is also no 
essential difference, although the distinction is convenient clinically. 

Symptoms. — The disease usually begins before puberty, but may be 
delayed until adolescence or early adult life (before the twenty-fifth year). 
The onset is insidious, the first symptoms being muscular weakness and 
disability, with or without increase in the volume of the muscles of the 
part. Depending upon the muscles involved, several clinical types of 
the disease are distinguished, although there is no sharp line of demarca- 
tion between them: (1) The pseudohypertrophic form of Duchenne. 
This usually develops before the tenth year and in males. It involves 
especially the muscles of the calves — which become much enlarged. The 
child in walking readily grows tired, stumbles, or drags the legs (in 
marked contrast to the healthy looking calves); and, to aid progression, 
soon begins to bring the pelvis into play, and develops a waddling gait. 
The muscles of the thigh, buttocks, and back soon become involved; the 
child experiences increasing difficulty in arising from a lying to a standing 
posture, and characteristically aids himself by "climbing up on his legs 
with his hands. " When erect, he stands with his legs apart, his shoulders 
thrown back (in an effort to compensate the forward curvature of the 
58 



914 DISEASES OF THE MUSCLES 

spine, due to atrophy of the lumbar muscles), and the abdomen protruded. 
The common enlargement of the muscles of the calves and of the anterior 
aspect of the thighs and the atrophy of the glutei muscles accentuate 
this attitude. Later, the muscles of the shoulder girdle may become in- 
volved. Muscles originally hypertrophied become atrophic, and con- 
tractures may ensue. Cases unassociated with the pseudohypertrophy 
are sometimes spoken of as the Leyden-Mobius form. (2) The scapulo- 
humeral form of Erb (Erb's juvenile form). This begins, as a rule, be- 
tween the ages of twelve and sixteen years, and involves first the muscles 
of the shoulder girdle, and then those of the upper arm and the anterior 
chest, and finally those of the back. In advanced cases the muscles of 
the thigh and calf become involved, so that the condition much resembles 
the pseudohypertrophic form of the disease. (3) The facioscapulo- 
humeral type of Landouzy and Dejerine. This begins in early childhood, 
in the third or fourth year, as a rule, and is especially characterized by 
atrophy of the muscles of the face, as well as of the muscles of the shoulder 
girdle and the upper arm (Erb's infantile form) ; the pseudohypertrophic 
type of Duchenne also may be associated. The lips protrude and can- 
not be closed, and their finer movements (articulation, puckering, re- 
taining fluid and food) are interfered with, although mastication and 
deglutition may be unimpaired. The ocular and palpebral muscles 
often escape. 

Diagnosis. — The different forms of muscular dystrophy are readily dis- 
tinguished by their hereditary or familial occurrence, their usual onset in 
early life, involvement of the muscles near to the trunk (rather than the 
small muscles of the hands and feet, as in progressive muscular atrophy), 
and the occurrence of pseudohypertrophy of certain muscles, especially 
the calves; by gradual reduction in the deep reflexes and electrical excita- 
bility of the muscles — depending upon the gradual muscular atrophy 
(the muscular fibers remaining continuing to respond); and by the 
absence of the reactions of degeneration, of fibrillary twitchings, and of 
sensory changes. These serve to exclude chronic poliomyelitis, progres- 
sive muscular atrophy, and multiple neuritis. 

Prognosis. — Muscular dystrophy is slowly progressive, but it may last 
twenty or thirty years, and does not lead directly to death. 

Treatment. — It is at least doubtful whether any treatment is really 
efficacious. Regulated exercises, passive movements, massage, elec- 
tricity, hydrotherapeutic measures, and tonics are serviceable in some 
cases. 

MYOCLONUS. 

(Paramyoclonus Multiplex, Friedreich.) 

Myoclonus is a disorder characterized by clonic, constant or paroxys- 
mal, contractions of the muscles, chiefly of the legs. The disease is 
sometimes hereditary; it may affect several members of the same family; 
it occurs especially in males, and it may be found in epileptic subjects. 



CONGENITAL MYOTONIA 915 

Its cause is not known; it is said to follow fright, shock, and general ill 
health. Its nature has not been determined; some observers believe it 
to be allied to the convulsive tics, electric chorea, etc. The characteristic 
symptoms consist of sudden electric-like, clonic contractions of the 
muscles, especially of the legs, sometimes of the trunk, and rarely of the 
face. The spasms, as a rule, are bilateral and rhythmic; they vary from 
50 to 150 per minute, and may be so violent as to cause motion of the 
entire limb, or even tossing about of the patient. They are often lessened 
by voluntary movement, and they usually cease during sleep. In the 
paroxysmal cases tremors of the muscles may occur during the intervals. 
The reflexes are usually exaggerated, the nutrition of the muscles is well 
maintained, and there are no reactions of degenerations, sensory changes, 
or psychic disturbances. The disorder may be distinguished from 
acute chorea by the sudden electric-like quickness of the movements and 
their occurrence especially in the legs, and from the convulsive tics, the 
movements of w T hich are purposeful and usually unilateral. The dis- 
order lasts a variable time, and may cease spontaneously. The treatment 
consists of the use of sedatives, such as the bromides, valerian, hyoscine, 
etc. 

CONGENITAL MYOTONIA. 

(Thomsen's Disease.) 

Congenital myotonia is a disease characterized by rigidity or tonic con- 
tractions of the muscles upon attempting voluntary movements after a 
period of rest. It is usually hereditary; it may affect several members 
of the same generation; it is almost ten times as common in males as in 
females, and it usually develops during childhood. The nature of the 
disorder is not known; it has been attributed to changes in the muscle 
fibers, to an auto-intoxication involving especially the muscles, etc. The 
nervous system shows no lesions. The symptoms consist of the occur- 
rence of tonic spasms of the muscles upon attempting voluntary move- 
ments — such as arising from a chair, walking, grasping an object, closing 
the eyelids, etc.; that is, the patient experiences difficulty and delay in 
initiating the movement, but, once begun, persistence in the movement 
results in relaxation of the contracted muscle; but a period of rest is fol- 
lowed by recurrence of the phenomena. This incapacitates the child 
more or less and prevents his engaging in children's plays and games. 
The muscles are usually well developed and may even appear hyper- 
trophied, but some muscular weakness is common, although there is 
no atrophy. The mechanical excitability of the muscles is increased — a 
blow, for instance, causing a quick and lasting contraction (ten to 
twenty seconds). The electrical excitability also is increased and occasions 
the so-called myotonic reaction: undue excitability to mild faradic and 
galvanic currents; rather slow maximum response to the current and slow 
relaxation; under the influence of the galvanic current the anode-closing 
contraction (ACC) becomes equal to or greater than the cathode-closing 



916 DISEASES OF THE MUSCLES 

contraction (CCC); and if a continuous galvanic current is passed through 
the muscle, rhythmic, vermicular contractions pass from the cathode to 
the anode. No efficacious treatment is known. 



CONGENITAL AMYOTONIA. 

(Congenital Myatonia; General or Localized Hypotonia of the Muscles of Children; 
Congential Hypotonic or Atonic Pseudoparalysis; Oppenheim's Disease.) 

Congenital amyotonia is a disease characterized by diminished tone 
(hypotonia) of the voluntary muscles. The disorder is undoubtedly 
congenital, and becomes manifest during childhood; infections are 
sometimes said to act as exciting causes. The nature of the condition is 
not known; changes in the muscles analogous to those of the muscular 
dystrophies have been found. The symptoms consist of flaccidity and 
loss of tone and power of the voluntary muscles, but there is no absolute 
paralysis and no wasting of the muscles. The condition is usually most 
marked in the limbs, and is often associated with relaxation of the joints, 
so that the limbs may be readily placed in grotesque positions and luxa- 
tions may ensue; but the muscles of the trunk and of the face may be 
involved. The deep reflexes are lessened or lost ; the electrical excitability 
is diminished, and currents much stronger than in health can be borne 
with equanimity. The disorder may be distinguished from the muscular 
dystrophies by its being congenital (but not hereditary) and non-familial, 
and by the marked hypotonia and absence of wasting of the muscles. It 
should be readily differentiated from acute poliomyelitis, rickets, etc. The 
prognosis is good, since the condition tends to lessen and finally to disap- 
pear as the child grows older, but contractures may occasionally occur. 
The treatment consists of hygienic and dietetic regulations designed to 
improve the general health and nutrition of the child, and of massage, 
electricity, and hydropathic measures to increase the tone of the muscles. 



SECTION XII. 
DISEASES OF THE BONES AND JOINTS. 



ACUTE ARTHRITIS. 

Etiology. — Acute arthritis, aside from, and often including, the cases 
that follow local injury, is always due to bacterial infection or intoxica- 
tion. It may occur as a primary disorder, of which the joint manifesta- 
tions are the conspicuous feature — rheumatic fever (page 253) ; or it may 
occur in the course of or following any of the well-known pyococcic, 
pneumococcic, gonococcic (page 91), influenzal, and other infections. 
Special importance attaches to unsuspected, masked, and more or less 
obsolete infections, such as tonsillitis, pyorrhoea alveolaris, chronic gono- 
coccic infection with involvement of the seminal vesicles and the pros- 
tate, other infections of the urinary tract, of the gastro-intestinal tract, etc. 

Pathology. — One or several joints may be involved. In the mild cases 
the lesions consist of congestion, swelling, and oedema of synovial tissues, 
and the outpouring into the cavity of the joint of a more or less turbid 
albuminous fluid containing a few flakes of fibrin and leukocytes. In 
more severe cases the synovial and fibrous capsules of the joints are 
swollen, oedematous, and adherent, and the cavity of the joint is filled 
up, perhaps obliterated, by more or less thick, fibrinous, fibrinopurulent, 
or distinctly purulent exudate; the articulating cartilaginous surfaces 
may reveal erosions with thickened infiltrated borders. In less severe 
and more chronic cases there may be more or less villous proliferation 
of the synovial tissue. The infecting microorganisms may sometimes be 
isolated from the articular fluid or tissues, but often having initiated the 
lesions they die out; or the lesions may be set up by bacterial toxins alone. 

Symptoms. — The onset of the disorder may be abrupt or more or less 
insidious, depending upon the severity of the infection. The chief 
symptoms consist of pain, tenderness, swelling, increased temperature, 
and disability of the joint or joints. On palpation the joint is soft and 
boggy — in consequence of more or less intra-articular fluid, swelling of 
the synovial tissues, and periarticular oedema. In addition, there are the 
general evidences of infection — due in part to the primary disorder, but 
perhaps aggravated by the local joint condition — fever, rapid pulse, and 
leukocytosis; in the event of suppuration, also chills or chilliness and 
sweats. 



918 DISEASES OF THE BONES AND JOINTS 

Diagnosis. — The diagnosis is quite apparent from the local conditions. 
Efforts should be made to determine the nature of the infection — by 
searching for sources of infection and cultivating therefrom the infecting 
microorganism, or, when the conditions appear to warrant it, aspirating 
the joint and studying the fluid bacteriologically and cytologically. 

Prognosis. — The prognosis depends upon the severity of the in- 
fection and the nature of the ensuing lesions. There is always a ten- 
dency for the condition to become polyarthritic, even in originally mon- 
arthritic cases, and in all but the mildest cases more or less permanent 
disability is likely to ensue. 

Treatment. — All possible local sources of infection anywhere in the 
body must be eradicated, since the joint symptoms may be kept active 
by bacterial toxemia without local joint infection. The best treatment 
comprises rest and fixation of the joint and the local remedies mentioned 
on page 257. The rest should not be too long continued, passive move- 
ments being substituted as soon as possible. Good results also may 
attend the use of specific bacterins. In cases of severe and progressive 
infections, resort should be had to surgical procedures — opening and 
irrigating and draining the joint. 



CHRONIC ATROPHIC ARTHRITIS. 

(Arthritis Deformans; Rheumatoid Arthritis; Chronic Polyarthritis of the Atrophic 

Type of Goldthwait.) 

Etiology. — The form of chronic polyarthritis known as deforming or 
rheumatoid arthritis (the atrophic type of Goldthwait), is a disease of 
adult life, and is more common in women than in men. Goldthwait 
discounts the likelihood of an infectious cause in these cases, emphasizing 
the etiological significance of poverty, wear and tear of life, grief, fear, 
severe nervous shock, and great physical and mental strain. These are 
undoubtedly present in many cases, and of unquestionable causative im- 
portance; but in many cases also, and in increasing numbers as the cases 
are the more carefully studied, some chronic unsuspected, masked, or 
concealed infection is found — in the tonsils, about the teeth, gleet, 
chronic gastro-intestinal infections, etc.; some cases represent an 
advanced stage of a disorder developed acutely and undoubtedly infec- 
tious; and Still has described a type of the disorder occurring in children, 
and characterized by enlargement of the lymph nodes and the spleen, in 
addition to the joint lesions. In some cases gastro-intestinal and other 
metabolic poisons may be an active factor. 

Pathology. — The lesions involve all the articular structures — the syn- 
ovial membrane and fluid, the cartilages, and the bone. The earliest 
changes consist of inflammatory and hypertrophic alteration of the syno- 
vial tissue, with the production of a condition called villous arthritis, and 
thickening, swelling, and infiltration of the peri-articular tissues. Grad- 
ually the inflammatory lesions of the synovial tissue subside, and cicatri- 



CHRONIC ATROPHIC ARTHRITIS 919 

zation and atrophy ensue. In the course of time the cartilage becomes 
opaque, striated, and atrophied, so that large or small erosions of the 
articular surfaces develop; opposed surfaces of exposed bone being 
brought into contact, give rise to rough, grating impressions; the bone 
trabecule become reduced in size and number, and other atrophic and 
rarefying changes ensue. The synovial fluid may be present in excess in 
the early stages, but late it is usually normal in amount, the increase in 
the size of the joint being due to thickening of the soft periarticular 
tissues. Osseous spurs may sometimes be seen (attempt at repair). 

Symptoms. — Chronic atrophic arthritis is a poly arthritic disorder that 
begins insidiously in the small joints of the hands — not always at the 
same time in both hands, but both soon become involved; later, the 
small joints of the feet, and the wrists, elbows, ankles, knees, shoulders, 
and other joints, even all the joints of the body, may become affected. 
A single joint is rarely involved alone. The patient at first experiences 
pain or difficulty in executing fine and complicated movements involving 
the hands; the phalangeal and metacarpophalangeal joints soon become 
swollen — due to periarticular oedema and infiltration, in part sometimes 
to increase of the synovial fluid. Deformities gradually ensue, which 
result in part from the swelling, in part from gradual atrophy of the 
articular tissues, and in part from subluxation and flexion (the stronger 
flexors overcoming the weaker extensors); lateral deformities also may 
ensue, notably ulnar deviation of the hands and knock-knees. Crepita- 
tion occurs on flexing and extending the joints (due to the rubbing of 
villi or erosions), and more or less fixation may result from the contrac- 
tion of muscles or bony ankylosis. The muscles about the joints usually 
atrophy. Fluctuation in the severity of the lesions occurs from time to 
time; and the condition may even abate or become quiescent. There 
are, as a rule, few general symptoms aside from general malnutrition and 
anemia. 

Diagnosis. — The symptoms are sufficiently distinctive to enable one to 
recognize the disorder. The lesions may be well studied by radiographic 
examination. 

Prognosis. — The outlook is not promising, although considerable ameli- 
oration of the condition may be brought about in the early stages. 

Treatment. — Sources of infection must be searched for and eradicated; 
and attention must be given to improving the general nutrition of the 
patient by good food, good air, rest, and freedom from distress and worry. 
Internally, syrup of iron iodide, cod-liver oil, arsenic, and thyroid extract 
are sometimes efficacious. Locally, belladonna, mercury, and iodine 
ointment, massage, electricity, passive movements, hydrotherapeutic 
measures, exposure to superheated air (" baking" the joints) render ser- 
vice. If there is much and persistent accumulation of fluid, it may be 
withdrawn. Care must be taken that flexions, subluxations, and other 
deformities do not ensue, and if ankylosis seems inevitable, that it occurs 
while the joints are in a position to permit of their being useful. Per- 
sistent and disabling deformities may be corrected by surgical methods. 



920 DISEASES OF THE BONES AND JOINTS 

CHRONIC HYPERTROPHIC OSTEO-ARTHRITIS. 

(Arthritis Deformans of the Hypertrophic Type of Goldthwait.) 

Etiology. — Goldthwait applies the term chronic hypertrophic arthritis 
to a "chronic constitutional disease with local joint manifestations, 
which may or may not be polyarticular." The disorder is more common 
in men than in women, and occurs in middle life and old age. The etio- 
logical factors are not well understood; some significance is attached to 
exposure; to injuries, which maybe single and severe and, involving one 
of the large joints, may apparently soon lead to the disease, or which may 
be slight, inconsequential, but frequently repeated and related to the 
patient's occupation; to gastro-intestinal derangements and consequent 
auto-intoxication; and to the changes of senility. 

Pathology. — The joints most commonly involved are the fingers, knees, 
vertebras, hips, and feet. The chief lesions consist of slight localized vil- 
lous hypertrophy of the synovial tissue and of the related cartilage; and 
of hypertrophy of the cartilage along the outer margin of the joint and 
that associated with the ligaments (so-called lipping). This hypertrophy 
consists of fairly normal cartilage (in contrast with the changes in the 
cartilage in the atrophic form of the disease); it is quite irregular in de- 
gree, and soon becomes ossified — that is, into it osteophytes develop 
(so-called Haygarth's nodosities at the knuckles); sometimes there is an 
associated bony spur formation or hyperplasia at the point of attach- 
ment of the ligaments and tendons. These together produce more or less 
joint disability and fixation. Erosions occur, but they result from the 
action of the osteophytes or from pressure, and they differ from those of 
the atrophic type of the disease in showing at their bottom eburnated 
cartilage and not exposed bone. 

Symptoms. — The onset of the disorder is slow, and considerable progress 
may be made before noteworthy symptoms supervene. The usual com- 
plaint is of articular discomfort and pain and more or less disability, all 
of which are increased on activity and improved on resting. From time 
to time the symptoms disappear, perhaps entirely, and leave no symptoms 
except the bony deformities. The condition is quite common in the 
hands, occurring as small, hard knobs of hypertrophied cartilage and 
bone at the dorsal or dorsolateral margin of the articulating surfaces of 
the terminal phalanges (Heberden's nodes). Flexion or lateral devia- 
tion of the terminal phalanges occurs from pressure atrophy on the side 
toward which the nodes push. The condition is incurable, but it brings 
with it the happy reflection that its subjects rarely become affected with 
disease of the larger joints. In the knees, considerable enlargement, of 
the femur, the tibia, and the patella, with subluxation and fixation of the 
joint (osteophyte formation) ensue, and the patient is often permanently 
disabled. In the hip (morbus coxae senilis) the changes involve the head 
of the femur and the acetabulum; the acetabulum becomes broadened 
and the upper lip grows over and may completely surround the neck of 



OSTEOMALACIA 921 

the femur, effectually limiting motion. In the vertebrae the lesions often 
involve several adjacent vertebras; the cartilaginous proliferation may 
extend to several neighboring bones, and the osteophyte proliferation 
may invade not only this but also the intervertebral cartilages, and may 
extend down the anterior and anterolateral aspects of the vertebrae, 
effectually ankylosing them (so-called spondylose rhizomelique). The 
condition is most common in the thoracicolumbar and the cervical ver- 
tebrae. It gives rise to more or less, often marked, rigidity of the ver- 
tebrae, and local pain; the pain often radiates (unusually unilaterally) 
to the area of distribution of the sensory roots that enter the vertebral 
column amidst the lesions. 

Diagnosis. — The disease is readily recognized. The articular lesions 
can be well studied by radiographic examination. 

Prognosis. — The outlook as to cure is not good. Once established 
the disease is irremediable, but some amelioration can be effected in the 
early stages. 

Treatment. — The treatment is that recommended for the atrophic form 
of the disease. Care should be taken to prevent deformities; if they 
develop they may be corrected by surgical methods. 



OSTEOMALACIA. 

(Mollities Ossium; Fragilitas Ossium.) 

Osteomalacia is a chronic disorder of nutrition characterized by decal- 
cification and progressive softening of developed and ossified bones, 
leading to bending or fracture and more or less deformity. 

Etiology. — The disorder is rare, but occurs, especially in adult life and 
in women (10 to 1 man). It is commoner among the poor than the 
well-to-do, and seems to be epidemic in certain regions (in Europe). It 
occurs most frequently in pregnant and nursing women, especially mul- 
tipara, but also in virgins (relation to ovulation '?) ; pregnancy may merely 
cause an exacerbation of the disease already existent. 

Pathology. — The bones most commonly affected are the pelvic bones, 
the vertebrae, and the ribs; the long bones usually are affected late. The 
lesions consist in decalcification of the compact and spongy parts of the 
bone and their replacement by a soft, vascular, gelatinous, sometimes 
hemorrhagic or cystic, tissue; the periosteum may be involved or thick- 
ened and hyperemic. The bones in consequence become softened or 
brittle, and, yielding to divers influences, become bent, distorted, and 
may be readily fractured. The nature of the disease is not known; a 
relationship between the osteomalacia (decalcification) of pregnancy and 
lactation and the need of the growing foetus and child for lime and phos- 
phorus has been postulated. An influence of the ductless glands also has 
been suggested; the parathyroids are known to have an influence on 
calcium metabolism (deficiency provoking tetany); the ovaries perhaps 
influence the absorption of calcium (and some cases of osteomalacia 



922 DISEASES OF THE BONES AND JOINTS 

have been cured by oophorectomy); the thyroids also have been impli- 
cated — but the exact interrelationship, if any, is not well understood. 

Symptoms. — The onset of the disease is insidious, and it may be far 
advanced when first recognized (as, for instance, vaginal examination at 
impending parturition). The earliest symptom usually is pain (misin- 
terpreted as rheumatic) in the pelvis, vertebras, thorax, legs, etc., perhaps 
associated with difficulty in locomotion (hobbling or wobbling gait). 
Gradually deformities develop; the sacral promontory and the acetabula 
approach one another (osteomalacic pelvis); lordosis, kyphosis, or sko- 
liosis ensues; the bones of the legs become curved (the patient often is obvi- 
ously growing shorter), and fractures may occur spontaneously or on very 
slight provocation. The cranium usually is not much, if at all, involved. 
The patient may become bedridden. The muscles are usually flaccid 
and atrophic (rarely spastic), and may exhibit fibrillary twitchings, 
intention tremors, etc. The urine contains an excess of calcium and 
phosphorus. 

Diagnosis. — The diagnosis often is not made until the disease is well 
advanced — when it presents no difficulties. In the early stage, muscular 
rheumatism and divers diseases of the bones and of the nervous system 
must be excluded. Attention to the possibility of the disease in a pregnant 
or nursing woman, examination especially of the pelvic bones for defor- 
mities, radiographic examination (for decalcification), and a study of 
the calcium output in the urine should enable the diagnosis to be made 
early in many cases. 

Prognosis. — The disease is usually progressive, running a course of five 
or ten years or more; sometimes the course is rapid — less than a year; 
sometimes it becomes arrested, and perhaps made worse by a subsequent 
pregnancy. Death usually ensues from progressive weakness or inter- 
current infection. 

Treatment. — The treatment is largely symptomatic: good food, 
good hygiene, and the avoidance of etiological factors — nursing in those 
already affected, as well as subsequent pregnancy. Calcium and phos- 
phorus (cod-liver oil and other phosphorus-bearing oils and foods) often 
are markedly beneficial. Improvement has followed the use of adrenalin 
to the point of toleration. Ovariotomy has led to improvement in ad- 
vanced cases in women. 



OSTEITIS DEFORMANS. 

(PageVs Disease.) 

Osteitis deformans is a rare disorder, characterized by "enlargement 
and forward projection of the head, dorsocervical kyphosis, prominence 
of the clavicles, spreading of the base of the thorax, a diamond-shaped 
abdomen crossed by a deep sulcus, a relative increase in the width of 
the hips, and an outward and forward bowing of the legs" (Packard, 
Steele, and Kirkbride). The subjects become notably reduced in height. 



FACIAL HEMIATROPHY 923 

The cause of the disease is not known; it is believed to be related to 
osteomalacia, and perhaps to disorders of the pituitary body and the 
other ductless glands. The lesions consist of a rarefying and formative 
osteitis. The diagnosis is apparent at a glance. Treatment seems to 
be inefficacious. 



HYPERTROPHIC PULMONARY OSTEO-ARTHROPATHY. 

Hypertrophic pulmonary osteo-arthropathy is a rare disorder, charac- 
terized by enlargement of the ends of the bones of the hands and feet, 
especially the terminal phalanges, and sometimes also of the distal ends 
of the long bones of the forearm and legs. The ends of the fingers 
become characteristically bulbous and the finger nails elongated and 
curved about them. The nature of the disease is not known. Most of the 
cases are associated with long-standing (usually suppurative) disorders 
of the lungs or pleura, and it has been supposed (Marie) that the toxins of 
the pulmonary disorder, reaching the bones by way of the circulation, 
set up an ossifying periostitis. A somewhat similar condition sometimes 
occurs in chronic heart disease, syphilis, tuberculosis; or it may develop 
from unknown causes. Freedom from involvement of the bones of the 
skull and face readily excludes akromegaly. 

OSTEOGENESIS IMPERFECTA. 

Osteogenesis imperfecta is a rare disorder, characterized by imperfect 
development of the bones, especially of the skull and the extremities. 
The bones are exceedingly fragile, so that intra-uterine and extra-uterine 
fractures are common. Should the child survive, ossification ultimately 
may become normal, although the bones may be more or less deformed. 

ACHONDROPLASIA. 

( Chondrodystrophia Foetalis . ) 

Achondroplasia is a disorder due to perverted development (dys- 
trophy) of the epiphyseal cartilages (connective-tissue invasion from the 
periosteum), in consequence of which the epiphyses and diaphyses become 
prematurely united and the normal growth of the long bones does not 
occur. The subjects are dwarfs, usually with normal heads and trunks, 
and short, stumpy extremities. 

FACIAL HEMIATROPHY. 

Facial hemiatrophy is a rare disorder, characterized by atrophy of the 
bones and soft tissues of one-half of the face. The nature of the disorder 



924 DISEASES OF THE BONES AND JOINTS 

is not well understood; interstitial neuritis of the entire trigeminal nerve 
has been found. The disorder begins usually in childhood, although it 
may come on later; and it may follow an injury or infection. There is 
gradual wasting of all the tissues, skin, subcutaneous connective tissues, 
and the bone, and to some extent also the muscles. The skin becomes 
pale, the hair whitens and may fall, and the teeth may drop out. There 
may be some associated sensory changes. The condition is readily 
recognized. 

LEONTIASIS OSSEA. 

Leontiasis ossea is a rare disorder, characterized by enlargement of the 
cranial, and sometimes the facial, bones — occasioning a so-called leontine 
expression. The nature of the disease is unknown. 



INDEX 



Abasia, 893 
Abdominal angina, 492 

typhus, 32 
Abducens nerve, 816 
Abnormal intestinal contents, 677 
Abscess of brain, 871 

of liver, 707 

of lung, 559 

peritonsillar, 599 

retropharyngeal, 604 

of spleen, 406 

subphrenic, 749 
Acanthocephaliasis, 221 
Acariasis, 224 
Acholia, 688 

Achondroplasia, 329, 923 
Achylia gastrica, 619, 620 
Acidosis and acid intoxications, 304 
Acroparesthesia, 908 
Actinomycosis, 169 
Activators, 338 
Adams-Stokes syndrome, 421 
Addison's anemia, 573 

disease, 353 

incomplete, 352 
Adenie, 397 

Adenoid vegetations, 601 
Adenolipomatosis, symmetrical, 328 
Adenoma, 349 
Adhesive pericarditis, 485 
Adiposis cerebralis, 328 

dolorosa, 327 

tuberosa, 328 
Adrenal glycosuria, 338 

inadequacy, 353 

insufficiency, 352 
Adrenals, diseases of, 351 
African blood fluke, 213 

lethargy, 194 

tick fever, 178, 224 
.Agglutinins, 21 
Aggressins, 22 
Agoraphobia, 895, 903 
Agraphia, 842 
Ague, 197 
Ainhum, 287 
Air and gas in pericardium, 488 

disease, compressed, 878 

-hunger, 508 
Akoria, 617 



Akromegaly, 355 
Albuminuria, 764 

accidental, 764 

adolescent, 765 

extrarenal, 764 

factitious, 764 

functional, 765 

physiological, 765 

spurious, 764 
Albumosuria, 767 
Alcoholism, 289 
Alexia, 841 
Alexin, 21 
Alkaptonuria, 758 
Amaurotic family idiocy, 847 
Amblyopia, hysterical, 815 
Amboceptors, 21 
Amnesia, 844 
Amcebiasis, 175 
Amoebic colitis, 175 

dysentery, 175 
Amyloid disease, 334 
Amyloidosis, 334 
Amyotonia, congenital, 916 
Amyotrophic lateral sclerosis, 852 
Anakhre, 287 
Anaphylaxis, 29 
Anemia, 361 

acute secondary, 365 

aplastic, 377 

chronic secondary, 367 

in children, 409 

infantum pseudoleukaemica of von 
Jaksch, 409 

miners', 218 

of brain, 861 

pernicious, 373 

splenic, 407, 408 
Aneurysm, 497 

diagnosis of, 501 

of heart, 443 

physical signs of, 500 

symptoms of, 498 

treatment of, 502 
Angina, 598 

abdominal, 492 

Ludovici, 597 

pectoris, 493 
Angioneurotic cedema, 907 
Angiosclerosis, 489 
Ankylostomiasis, 218 
Anopheles, 198 



926 



INDEX 



Anorexia, 617 
Anosmia, 814 
Anthracosis, 554 
Anthrax, 161 

oedema, malignant, 162 
Antibodies, 20 

specific, 21 
Antigen, 20, 21 
Antilysin, 21 
Anuria, 763 
Aortic insufficiency, 462 

stenosis, 466 
Aortitis, acute, 489 
Aphasia, 840 

types of, 841 
Aphemia, 642 
Aphthae of palate, 591 
Aphthous fever, 273 
Aplastic anemia, 377 
Apneumatosis, 547 
Apoplexy, 862 

pulmonary, 545 
Appendicitis, 668 
Apraxia, 843 
Aprosexia, 601 
Aptyalism, 596 
Arithmomania, 903 
Arrhythmia, cardiac, 416 
Arrhythmic breathing, 509 
Arsenical poisoning, 296 
Arteries, diseases of, 489 
Arterio-capillary fibrosis, 489 
Arteriosclerosis, 489 

hypertrophy of heart in, 439 

nodose, 489 

senile, 490 

syphilitic, 490 
Arteriosclerotic kidney, 783 
Arthritis, acute, 917 

chronic atrophic, 918 
hypertrophic, 920 

deformans, 918 

gonococcic, 91 
Ascariasis, 219 
Ascites, 746 
Asiatic blood fluke, 213 

opisthorchiasis, 211 
Aspergillosis, pulmonary, 171 
Asphyxia, 510 

local, 908 
Astasia, 893 
Astereognosis, 844 
Asthenia, cardiac, 424 
Asthma, bronchial, 534 

cardiac, 413 

Kopp's, 404 

Millar's, 404 

spasmodic, 534 

thymic, 403 
Ataxic paraplegia, 858 
Atelectasis of lung, 547 
Ateliosis, 336 
Atheroma, 489 
Atherosclerosis, 489 



Athlete's heart, 427 
Athyrea, 339 

Atypical actinomycosis, 171 
Auditory nerve, 819 

vertigo, 819 
Aura asthmatica, 535 

epileptica, 889 
Auricles, hypertrophy of, 442 
Auricular extrasystoles, 417 
Auriculo ventricular extrasystoles, 418 
Auto-intoxication, acid, 304 

duodenal, 304 

gastro-intestinal, 303 

retention, 305 
Autumnal catarrh, 515 
A virulent diphtheria, 135 
Azotorrhoea, 737 



Baccelli's sign in pleuritis, 569 
Bacillary dysentery, 145 
Bacteremia, 22, 61 

gonococcic, 90 

typhoid fever, 34 
Bacteria, pathogenic, 20 
Bacterial infection, 32 

intoxication, 22 

protein, 21 

vaccines, 32 
Bacterins, 32 
Bacteriolysins, 21 

Bamberger's sign in pericarditis, 481 
Banti's disease, 408 
Barlow's disease, 333 
Bartender's paralysis, 823 
Basedow's disease, 342 
Basophilia, 364 
Bed-bugs, 225 
Bednar's aphthae, 591 
Beef tapeworm, 216 
Bell's palsy, 818 

Bence- Jones albumosuria, 401, 767 
Bends, the, 878 
Beriberi, 275 
Biermer's anemia, 373 
Big jaw, 169 
Bigeminal pulse, 418 
Bilharziosis, 213 
Biliary ducts, diseases of, 721 

obstruction of, 732 

fistula, 733 
Birth palsies, 846 
Black tongue, 595 
Blackwater fever, 208 
Bladder, inflammation of, 788 

tuberculosis of, 121 

tumors of, 799 
Blastomycetic dermatitis, 172 
Blastomycosis, 172 
Blood and hemopoietic system, d 

of, 359 
Blood-fluke disease, 213 



INDEX 



927 



Boit's breathing, 509 

Bone marrow, tuberculosis of, 102 

Bones and joints, diseases of, 917 

tuberculosis of, 124 
Boulimia, 611, 617 
Brachial plexus, 821 
Bradycardia, 422 
Brain, 832 

abscess of, 871 

anemia of, 861 

diffuse and focal diseases of, 861 

hyperemia of, 861 

localization of disease, 831 

non-system diseases of, 859 

oedema of, 862 

system diseases of, 845 

tumors of, 873 
Break-bone fever, 265 
Breast-pang, 493 
Bridal paralysis, 823 
Bright's disease, acute, 773 
chronic, 780, 783 
Brissaud's type of infantilism, 336 
Broadbent's sign in diseases of pericar- 
dium, 486 
Bromatotoxism, 299 
Bronchi, diseases of, 524 
Bronchial asthma, 534 

catarrh, acute, 524 
chronic, 527 
Bronchiectasis, 532 
Bronchiolectasis, 533 
Bronchiolitis exudativa of Curschmann, 

535 
Bronchitis, acute, 524 

capillary, 549 

chronic, 527 

fetid, 528 

fibrinous, 529 

gouty, 528 

putrid, 528 

with emphysema, chronic, 528 
Bronchocele, 340 
Bronchopneumonia, 549 
Bronchopulmonary hemorrhage, 539 
Bronchorrhcea, 529 
Brown-Sequard paralysis, 838 
Bruit d'airain of Trousseau, 582 

de diable, 368, 371 

de drapeau, 532 

de rappel, 461 
Bubo, parotid, 596 

tropical, 283 
Bubonic plague, 156, 157 
Bulbar palsy, acute, 850 
asthenic, 851 
chronic, 850 
Buhl's disease, 387 



Cachexia, chronic malarial, 203, 209 
lead, 295 
parastrumipriva, 349 



Cachexia, tropical, 195 
Caisson disease, 878 
Calabar swellings, 224 
Calculi, biliary, 728 

pancreatic, 745 

renal, 794 

salivary, 597 
Calmette's conjunctival test, 126 
Camp fever, 237 
de la Camp's sign in tuberculosis of lymph 

nodes, 101 
Cancrum oris, 593 
Capillary bronchitis, 549 
Carcinoma of gall-bladder and biliary 
ducts, 736 

of intestine, 676 

of larynx, 523 

of liver, 719 

of oesophagus, 607 

of pancreas, 744 

of peritoneum, 747 

of stomach, 638 

of thyroid, 349 
Cardarelli's sign in aneurysm, 499 
Cardia, spasm of, 615 
Cardiac asthenia, 424 

asthma, 413 

cirrhosis, 710 

pain, 415 

strain, 427 

type of infantilism, 336 
Cardialgia, 617 
Cardio-renal disease, 783 
Cardiovascular changes in nephritis, 760 
Catarrh, autumnal, 515 

dry chronic, 528 

sec, 528 
Catarrhal bronchitis, 527 

cholangitis, acute, 722 
chronic, 725 

fever, epidemic, 143 

gastritis, acute, 622 
chronic, 626 

jaundice, 722 

laryngitis, 517 

tonsillitis, 599 
Cellulocutaneous plague, 158 
Central ovale, lesions of, 834 
Cephalic tetanus of Rose, 151 
Cerebello-pontine angle, tumors of, 837 
Cerebellum, lesions of, 837 
Cerebral disorders, 832 

embolism, 869 

hemorrhage, 862 

meningeal hemorrhage, 825 

meninges, tuberculosis of, 122 

palsies of children, 846 

softening, 868, 869 

thrombosis, 868 
Cerebrospinal fever, 86 

localization, 831 

meninges, diseases of, 825 

meningitis, epidemic, 86 
Cervical myelitis, transverse, 880 



928 



INDEX 



Cervical plexus, 821 

rib, 822 

sympathetic nerves, diseases of, 824 
Cervico occipital neuralgia, 821 
Cestode infection, 214 
Chalicosis, 554 
Chancre, hard, 181 

Hunterian, 182 
Charbon, 161 

Charcot-Leyden octahedral crystals, 535 
Charcot's disease, 852 
Chattering teeth, 817 
Cheek, gangrene of, 593 
Cheese poisoning, 299 
Cheyne-Stokes breathing, 413, 509 
Chicken-pox, 235 
Chills in typhoid fever, 40 
Chloranemia, 369 

Chloroform poisoning, delayed, 699 
Chloroma, 383 
Chlorosis, 369 

Egyptian, 218 
Choked disk, 815 
Cholangitis, acute catarrhal, 722 

chronic catarrhal, 725 
. suppurative, 724 
Cholecystitis, acute, 726 

chronic, 728 
Cholelithiasis, 728 

complications and sequels of, 733 

diagnosis of, 733 

etiology of, 728 

pathology of, 729 

prognosis of, 734 

symptoms of, 730 

treatment of, 735 
Cholemia, 688, 694 
Cholera, 153 

Asiatic, 153 

infantum, 661 

morbus, 657 

nostras, 155, 657 

sicca, 155 
Cholerine, 155 
Choluria, 758 

Chondrodystrophia fcetalis, 925 
Chorea, acute, 900 

chronic progressive, 902 

habit, 901 

hereditarjr, 902 

insaniens, 901 

malignant, 901 

minor, 900 

senile, 904 
Choreiform disorders, 904 
Chromaffin system, 351 
Chvostek's sign in tetany, 351 
Chylopericardium, 488 
Chylothorax, 583 
Chylous ascites, 223 

diarrhoea, 223 
Chyluria, 758 

Circulatory system, diseases of, 411 
tuberculosis of, 106 



Cirrhosis, atrophic, 710 

biliary, 710, 717 

capsular, 709 

Hanot's, 710 

hypertrophic, 710 

Laennec's, 710 

monolobular, 710 

multilobular, 710 

of liver, 709 

portal, 710 

ventriculi, 627 
Cladothricosis, 171 
Cleithrophobia, 895, 903 
Clergymen's sore throat, 603 
Coal miner's disease, 554 
Cocaine habit, 293 
Coccidiaria, 174 
Coccidioidal granuloma, 172 
Coccygodynia, 809 
Cochlear nerve, 819 
Cceliac disease, 664 
Cold, common, 512 
Colic, lead, 295 

mucous, 654 

painter's, 295 
Colitis, mucous, 654 
Collapse of lung, 547 
Colles' law, 181 
Collier de Venus, 184 
Colon, dilatation of, 682 
Coloptosis, 685 

Combined system diseases, 857 
Complement, 21 
Completing substance, 21 
Compression of lung, 547 
Congestion of kidneys, 770 

of liver, 702, 703 

of lungs, 541 

of spleen, 407 
Constipation, 655 
Consumption, 92 
Conus medullaris, 880 
Convulsive tics, 903 
Coprolalia, 903 
Coprostasis, 677 
Corona veneris, 184 
Coronary arteries, diseases of, 444 
Corpora quadrigemina, lesions of, 836 
Corrigan's water-hammer pulse, 465 
Coryza, 512 
Costiveness, 655 
Cough, winter, 527 

Coughing in diseases of respiratory sys- 
tem, 510 
Cowpox, 233 

Cramps, occupation or professional, 897 
Cranial nerves, diseases of, 814 
Craniotabes, 330 
Craw-craw, 224 
Cretinism, 336, 346 
Croup, 135 
false, 520 
membranous, 137 
spasmodic, 520 



INDEX 



929 



Croupous or diphtheritic enteritis, 667 

pneumonia, 24, 71 
Crus, lesions of, 836 
Cryoscopy, 762 
Cryptogenetic infections, 63 
Culex, 198 

Curschmann's spirals, 535 
Cyanosis, 413, 510 

enterogenous, 304, 414 
Cyclic albuminuria, 765 

or periodic vomiting, 615 
Cycloplegia, 816 
Cylindruria, 768 
Cynanche gangrenosa, 597 
Cystic duct, obstruction of, 732 

kidneys, congenital, 797 
Cysticercus cellulosa, 218 
Cytase, 21 
Cytolysins, 21 
Cystinuria, 758 
Cystitis, 788 
Cysts of kidney, 797 

of pancreas, 743 



Dalrymple's sign in exophthalmic goitre, 

343 
Dandy fever, 265 

Dejerine's interstitial hypertrophic and 
progressive neuritis of infants, 814, 856 
Delhi boil, 196 
Delire de toucher, 903 
Delirium tremens, 290 
Dengue, 265 
Depression of conductivity, 420 

of contractility, 421 
Dermatitis coccidioides, 172 
Dermatomyositis, 912 
Deviation of the complement, 28 
Diabetes insipidus, 318 
mellitus, 305 

complications of, 311 
diagnosis of, 312 
diet list for, 314 
etiology of, 305 
pathology of, 305 
prognosis of, 313 
symptoms of, 308 
treatment of, 313 
Diarrhoea of children, 661 
hill, 280 
nervous, 647 
tubular, 654 
Diarrhceal disorders of children, 661 
Dibothriocephalus latus/ 215 
Dicrocoeliasis, 212 
Diet in diabetes, 314 

in typhoid fever, 52 
Dietetic albuminuria, 765 
Digestive system, diseases of, 587 

tuberculosis of, 117 
Dilatation of colon, 682 

59 



Diphtheria, 131 

avirulent, 135 

bacillus, variation in virulence of, 135 

complications and sequels of, 138 

diagnosis of, 139 

etiology of, 131 

laryngeal, 137 

malignant, 137 

nasal, 137 

pathology of, 132 

pharyngeal, 136 

prognosis of, 140 

symptoms of, 136 

treatment of, 140 

wound, 138 
Diphtheroid infections, 135 
Distomatosis, 211 
Distomiasis, 211 
Dittrich's plugs, 528 
Diverticula of oesophagus, 606 

of sigmoid, 672 
Diverticulitis, sigmoid, 672 
Dourine, 174 
Dracunculosis, 223 
Dropsy, epidemic, 277 

pericardial, 487 

peritoneal, 746 

pleural, 579 
Dry mouth, 596 
Dubini's electrical chorea, 904 
Ductless glands, diseases of, 337 
Duke's so-called fourth disease, 251 
Dum-dum fever, 195 
Durosiez's sign in heart disease, 466 
Dysentery, bacillary, 145 

amoebic, 175 

infantile, 661 
Dyspepsia, acute, 622 

chronic, 626 

intestinal, 650 

nervous, 621 
Dyspeptic diarrhoea, acute, 661 
Dyspnoea, 413, 508 
Dysthyreosis, 339 
Dystrophia adiposo genitalis, 328 
Dystrophy, progressive muscular, 912 

facio-scapulo-humeral type 
of Landouzy and De- 
jerine, 914 
Leyden-Mobius form, 914 
pseudohypertrophic form of 

Duchenne, 913 
scapulo-humeral form of 
Erb, 914 
Dystrypsia, 650 



Ebstein's sign in pericarditis, 481 
Echinococcus cyst, 349 

granulosa, 217 
Echokinesis, 903 
Echolalia, 903 
Eczema of tongue, 595 



930 



INDEX 



Eelworm infection, 219 
Egyptian chlorosis, 218 
Electrical conductivity of urine, 763 

reactions, 807 
Elephantiasis, 395 

of leg, 223 
Ellis and Garland, S-shaped curve of, 568 
Elongation of uvula, 604 
Embolism of mesenteric arteries, 682 
Emphysema, 555 

acute vesicular, 558 

interalveolar, 558 

interlobular, 558 

interstitial, 558 

large lunged, 555 

pseudohypertrophic, 555 

senile, 558 

subpleural, 558 

vicarious, 558 
Empyema, 574 

necessitatis, 575 

of pericardium, 483 

pulsating, 575 
Encephalitis, acute hemorrhagic, 871 
suppurative, 371 

cerebellar, 871 
Encephalopathy, lead, 295 
Endarteritis, chronic deforming, 489 
Endocardium, diseases of, 445 
Endocarditis, acute, 445 

chronic, 450 

gonococcic, 91 
Endophlebitis, chronic obliterating he- 
patic, 696 
portal, 697 
Endotheliolysins, 21 
Endothelioma, 397 

primitive, of spleen, 408 
Endotoxins, 21 
Enteralgia, 649 
Enteric fever, 32 
Enteritis, acute, 657 

chronic, 659 

croupous or diphtheritic, 667 

phlegmonous, 667 

pseudomembranous, 654 
Enterocolitis, 661 
Enterodynia, 649 
Enteroptosis, 685 
Enterorrhagia, 652 
Enzyme, fat-splitting, 609 
Eosinophilia, 364 
Epilepsy, 888 

Epileptiform convulsions, 888 
Epistaxis, 511 

recurring, 511 
Epstein-Pel disease, 400 
Epizootic aphtha, 273 
Ergotism, 300 

Erb's juvenile form of muscular dys- 
trophy, 914 

sign in tetany, 351 

upper arm type of brachial paralvsis, 
821 



Erni's tapotage sign in tuberculosis of 

lungs, 114 
Erysipelas, 67 

Erysipeloid of Rosenbach, 69 
Erythema, infectious, 251 

migrans, 69 
Erythremia, 385 
Erythrocytosis, 385 
Erythronielalgia, 907 
Estivo-autumnal malarial fever, 197 
infections, 203, 205 
parasite, 201 
Exan thematic typhus fever, 237 
Extrasystoles, auricular, 417 

nodal, 418 

ventricular, 417 



Facial nerve, 817 

paralysis, central, 817 
peripheral, 818 

spasm, 818 
Famine fever, 178, 237 
Farcy, 159 
Fascioliasis, 212 

Fatty tumors, multiple symmetrical, 328 
Fauces, diseases of, 598 
Faucitis, acute, 598 
Fecal impaction, 677 
Fetid bronchitis, 528 
Fever in infections, 25 
Fibrinous bronchiolitis, acute obliter- 
ating, 531 

bronchitis, 530 

pneumonia, 71 

rhinitis, 137 
Fibrinuria, 758 
Fibroid induration of lung, 552 

phthisis, 552 

pneumonia, chronic, 552 

tuberculosis, chronic, 115 
Fibrotic nutmeg liver, 703 
Filariasis, 223 
Fish poisoning, 300 
Fisher's sign in diseases of pericardium, 

487 
Flagellata, 173 
Flajani's disease, 342 
Fleas, 225 

Flexner's antimeningococcic serum, 32 
Flint murmur, 461, 466 
Fluke infections, 211 
Folie de doute, 903 
Follicular tonsillitis, 599 
Foot-and-mouth disease, 273 
Foot-drop, 812 
Food poisoning, 299 
Fourth disease, Duke's so-called, 251 
Fraentzel murmur, 461 
Frambcesia, 193 
Friedreich's ataxia, 857 

sign in diseases of pericardium, 486 
in tuberculosis of lungs, 114 



INDEX 



931 



Galactotoxism, 299 
Gall-bladder and biliary ducts, diseases 
of, 721 

carcinoma of, 736 

inflammation of, 726 
Gall sickness, 174 
Gallstones, 728 
Galziekte, 174 
Gambian horse disease, 174 
Gangosa, 286 
Gangrene of cheek, 593 

of lung, 561 

symmetrical, 908 
Gangrenous proctitis, 281 
Gaseous distention of the parotid duct, 

597 
Gastralgia, 617 
Gastrectasis, 630 
Gastric catarrh, acute, 622 
chronic, 626 

fever, 623 

neurasthenia, 621 
Gastritis, acute, 622 

chronic, 626 

infectious, 625 

phlegmonous, 624 

simple, 622 

suppurative, 624 

toxic, 624 
Gastrodynia, 617 
Gastro-enteritis of children, 661 
G astro-intestinal auto-intoxication, 303, 
661 

catarrh, 661 
Gastroptosis, 685 
Gastrorrhagia, 613 
Gastrosuccorrhcea, 619 
Gastroxynsis, 619 

Gaucher type of splenomegaly, 408 
Genito-urinary svstem, tuberculosis of, 

120 
Gerhardt's sign in tuberculosis of lungs, 

114 
Glanders, 159 
Glandular fever, 252 
Glenard's disease, 685 
Gliosis, spinal, 884 
Glossitis, 594 

Glossopharyngeal nerve, 819 
Glycosuric test, 762 
Gibraltar fever, 164 

Gilford's sign in exophthalmic goitre, 343 
Gigantism, 355 
Gilford's cases of dwarfs, 336 
Gilles de la Tourette's disease, 903 
Goitre, 340 

exophthalmic, 342 
Gonococcic bacteremia, 90 

endocarditis, 91 

infection, 90 

synovitis and arthritis, 91 
Goundou, 287 



Gout, 320 

acute, 323 

chronic, 324 

irregular, 325 

retrocedent, 324 

suppressed, 324 
Gouty bronchitis, 528 
von Graefe's sign in exophthalmic goitre, 

343 
Grain poisoning, 300 
Grancher's sign in tuberculosis of lymph 

nodes, 101 
Granuloma of genitals, ulcerating, 283 
Graves' disease, 342 
Green sickness, 369 
Grinder's rot or asthma, 554 
Grip, 143 

Grocco's triangle, 569 
Gruber-Widal reaction, 21, 28, 47, 49 
Grubler's tumor, 295 
Guinea-worm infection, 223 



H 



Hsemosporidia, 174 

Hall's sign in aneurysm, 499 

Halteridium, 174 

Halzoun, 212 

Harrison's groove, 330 

Hay asthma or fever, 515 

Haygarth's nodosities, 920 

Headache, bilious or sick, 886 

Heart, absolutely irregular, 419 

acute dilatation of, 438 

aneurysm of, 443 

block, 420, 423 

chronic dilatation of, 438 

enlargement of, 437 

fatty, 430 

fibroid, 434 

functional capacity of, 414 

hypertrophy and dilatation of, 437 
438 

infectious febrile, 431 

insufficient, 425 

irritable, 429 

neuromuscular disorders of, 415 

overstrained, 429 

palpitation of, 416 

-pang, 493 

parasites of, 444 

rupture of, 444 

valvular disease of, 452 

weak, 424 
Heat cramps, 905, 906 

exhaustion or prostration, 905 

stroke, 905 
Heberden's nodes, 920 
Hectic fever in pulmonary tuberculosis 

112 
Heel, painful, 810 
Hemarthrosis, 391 
Hematemesis, 613 



932 



INDEX 



Hematomyelia, 876 
Hematoporphyrinuria, 758 
Hematuria, 769 

Bilharzian, 213 

Egyptian, 213 
Hemeralopia, 815 
Hemiatrophy, facial, 923 
Hemiacrania, 886 
Hemiplegia, 862 

of infants, 846 
Hemisystole, 418 
Hemogenesis, deficient, 23, 362 
Hemoglobinuria, epidemic, 387 

malarial, 208 
Hemoglobinuric fever, 208 
Hemolymph nodes, 393 
Hemolysins, 21 
Hemolysis, 21 

increased, 362 
Hemolytic ictero-anemia, 692 
Hemopericardium, 487 
Hemophilia, 390 
Hemopneumothorax, 580 
Hemoptysis, 539 

parasitic, 211 
Hemothorax, 576, 580 
Henoch's hysterical chorea, 904 

purpura, 389 
Hemorrhage, bronchopulmonary, 539 

cerebral, 862 

from lenticulostriate artery, 864 

from stomach, 613 

in newborn, 387 

into cerebellum, 866 

into crus, 865 

into internal capsule, 864 

into pancreas, 737 

into pons and medulla, 866 

into spinal cord, 876 

pulmonary, 539 
Hemorrhagic cortical encephalitis, acute, 
871 

diseases, 387 

encephalitis, acute, 871 

infarction of lung, 545 

pachymeningitis, internal, 827 

pleuritis, 576 
Hemorrhoidal phlebectasis, 683 
Hemorrhoids, 683 
Hepatargia, 688 
Hepatic artery, diseases of, 696 

auto-intoxication, 688 

capsulitis, 709 

veins, diseases of, 696 
Hepatitis, acute, 705 

non-suppurative, 705 

chronic interstitial, 709 

suppurative, 707 
Hepatolysins, 21 
Hepatoptosis, 685 

partial, 695 
Hepatopulmonary abscess, 709 
Hereditary ataxia, 857 

cerebellar ataxia, 857 



Hereditary spastic paraplegia, 847, 
857 

spinal paralysis, 847 
Herpes zoster, 813 
Hertel's exophthalmometer, 343 
Hertoghe's hypothyroidism, 336 
Hiccough, 510 
Hill diarrhoea, 280 
Hippocratic succussion splash, 582 
Hirschsprung's disease, 682 
Hodgkin's disease, 397, 398 
Hoffmann's sign in tetany, 351 
Hookworm disease, 218 
Hormones, 338 
Hunterian chancre, 182 
Huntington's chorea, 902 
Hutchison's teeth, 189 

triad of symptoms in syphilis, 189 
Hydatid disease, 214 
Hydrargyrism, 297 
Hydrocephalic cry, 830 
Hydrocephalus, 875 
Hydronephrosis, 793 
Hydropericardium, 487 
Hydroperitoneum, 746 
Hydrophobia, 266 
Hydrotherapy in treatment of typhoid 

fever, 53 
Hydrothorax, 579 
Hymenolepsis nana, 216 
Hyperacidity, 618 
Hyperchlorhydria, 618 
Hyperemia of brain, 861 

of kidneys, 771 

of liver, 703 

of lungs, 541 
Hyperesthesia of stomach, 616 
Hypermotility or hyperkinesis of stomach, 

614 
Hypernephroma, 353, 798 
Hyperorexia, 617 
Hyperosmia, 814 
Hyperpituitarism, 355 
Hyperpncea, 508 
Hyperthyroidism, 339 

and exophthalmic goitre, 342 
Hypertrophic pulmonary osteoarthrop- 
athy, 923 

stenosis of pylorus, 643 
Hypochlorhydria, 619 
Hypochylia gastrica, 619 
Hypoepinephry, 353 
Hypoglossal nerve, 820 
Hypoosmia, 814 
Hypoparathyreosis, 349 
Hypophysis cerebri, 355 
Hypopituitarism, 355 
Hypostatic congestion of lungs, 542 
Hypothyroidism, 339, 346 
Hypotonia of muscles of children, general 

or localized, 916 
Hypotonic or atonic pseudoparalysis, 

congenital, 916 
Hysteria, 892 



INDEX 



933 



Ichthyosis of tongue, 595 
Ichthyotoxism, 300 
Icterus gravis, 691, 699, 705 

melas, 692 

neonatorum, 691 
Idiopathic hypertrophy of heart, 440 
Ileocolitis, 661, 663 
Ileus, 675 

paralytic, 675 
Immune bodies, 71 
Impulsive tic, 903 
Indian liver-fluke disease, 212 
Indigestion, chronic, 626, 636 

intestinal, 650 
Indigo-carmine test, 762 
Indurative mediastinopericarditis, 485 
Infantile dysentery, 661 
Infantilism, 335, 355 
Infarction of mesenteric vessels, 682 
Infection carriers, 19 
Infections, concurrent, 20 

diagnosis of, 28 

double, 20 

general, 63 

local, 63 

mixed, 20 

nature and lesions of, 20 

of unknown or doubtful etiology, 226 

pathological physiology of, 23 

pathways of, 19 

prophylaxis of, 29 

pyogenic, 61 

secondary, 20, 64 

terminal, 64 

treatment of, 31 
Infectious and contagious diseases, 17 

chorea, 900 

diseases, 17 

febrile heart, 431 

gastritis, 625 

lesions of biliary tract and adjacent 
viscera, 733 

phlegmon of pharynx, acute, 604 
Inflation, compensatory, of lungs, 558 
Influenza, 143 
Infusoria, 174 
Insolation, 905 

Intellectual centre of language, 843 
Intercortical sensory aphasia, 842 
Intermittent albuminuria, 765 

claudication or lameness, 493 

fever, 197 
Internal capsule of brain, 834 
Interstitial hypertrophic progressive neu- 
ritis of childhood, 814, 856 

nephritis, chronic, 783 

pneumonitis, chronic, 552 
Intestinal catarrh, 657 

colic, 649 

dyspepsia, 650 

-fluke disease, 212 

hemorrhage, 652 



Intestinal hemorrhage, in typhoid fever, 
42 

indigestion, 650 

infantilism, 304, 336 

juice, 645 

neuralgia, 649 

obstruction, 674, 733 

pain, 649 

sand, 683 

teniasis, 214 

tormina, 647 
Intestine, constriction of, 675 

diminished sensibility of, 650 

functional disorders of, 646 

incarceration of, 675 

intussusception or invagination of, 
675 

motor disorders of, 648 

occlusion of, 674 

paralysis of, 648 

paresthesia of, 650 

pathological physiology of, 643 

spasm of, 648 

stenosis of, 675 

strangulation of, 675 

stricture of, 675 

tuberculosis of, 118 

tumors of, 676 

ulceration of, 673 
Intoxication, acid, 304 

auto-, 304 

bacterial, 22 
Intoxications, 289 
Intrapleural pressure, 505 
Intraspinal hemorrhage, 876 
Iridoplegia, 816 
Ischemic paralysis, 823 
Itch, grain or straw-bed, 225 

sarcoptic, 224 
Ixodiasis, 224 



Jacksonian epilepsy, 890 
von Jaksch's disease, 400 
Jail fever, 237 
Japanese liver-fluke disease, 211 

river fever, 278 
Jaundice, 689 

acholuric, 692 

acute infectious, 272 

black, 692 

catarrhal, 722 

chronic family, 692 

congenital hemolytic, 692 

effects of, 692 

emotional, 691 

epidemic, 691 

grave, 691 

hemohepatogenous, 690 

hemolytic, 690 

hereditary, 692 

infectious, 690 

mechanical, 689 



934 



INDEX 



Jaundice, menstrual, 691 

obstructive, 689 

splenomegalic, 692 

toxic, 690 

types of, 689 

urobilin, 493 
JofTroy's sign in exophthalmic goitre, 344 
June cold, 515 
Juvenile arrhythmia, 416 



Kahler's disease, 401, 767 

Kakke, 275 

Kala-azar, 195 

Keratosis, 595 

Kidneys, active congestion of, 770 

acute hematogenous infection of, 779 

anomalies of form and position of, 770 

circulatory disturbances of, 770 

cysts of, 797 

functional capacity of, 762 

inflammation of, 772 

of pregnancy, 774 

parasitic cyst of, 797 

passive congestion of, 771 

solitary cyst of, 797 

tumors of, 798 
Kinases, 338 

Klumpke's paralysis, 822 
Kocher's sign in exophthalmic goitre, 343 
Kopp's asthma, 404 
Koranyi's triangle, 569 
Korsakoff's psychosis, 290, 812 
Kreatoxism, 299 
Kubisagari, 285 
Kussmaul's dyspnoea, 311, 509 

sign in disease of pericardium, 486 



La grippe, 143 
La perleche, 591 
Lacunar tonsillitis, 599 
Laennec, perles of, 535 
Lamblia intestinalis, 174 
Lancet-fluke infection, 212 
Landolfi's sign in heart disease, 466 
Landry's paralysis, 881 
Lardaceous disease, 334 
Laryngeal catarrh, 521 

diphtheria, 137 

perichondritis, 522 

tuberculosis, 107 
Laryngismus stridulus, 520 
Laryngitis, acute, 517 

chronic, 521 

cedematous, 519 

sicca, 518 

spasmodic, 520 
Larynx, diseases of, 517 

tumors of, 523 



Latent and masked malarial infection* 

209 
Lateral sclerosis, 845 
Lathyrism, 300 
Lead colic, 295 

poisoning, 294 
Leber's disease, 815 
Leishmania, 174 
Leontiasis ossea, 924 
Lepra alba, 167 
Leprosy, 166 
Leptomeningitis, 828 
Leukanemia, 377 
Leukemia, 378 

atypical, 383 

lymphatic, 378 

lymphocytic, 381 

lymphoid, 381 

medullary, 378 

myelocytic, 379 

myeloid, 379 

splenic, 378 
Leukocythemia, 378 
Leukocytosis, 362, 364 

pathological, 364 

physiological, 364 
Leukoma, 595 
Leukopenia, 362, 363 
Leukoplakia, 595 

oris et buccalis, 595 
Leukosarcoma, 397 
Levulosuria, alimentary, 688 
Lingual tonsils, 604 
Linguiform lobe of the liver, 695 
Lipase, 609 
Lipomatosis, multiple, 328 

symmetrical, 327 
Lipuria, 758 
Lissauer's tract, 853 
Little's disease, 846 
Liver, abscess of, 707 

active congestion of, 702 

acute yellow atrophy of, 698, 705 

anomalies of form and position, 695 

carcinoma of, 719 

cardiac, 703 

cirrhosis of, 709 
biliary, 717 
portal, 710 

congested nutmeg, 703 

corset or constricted, 695 

diseases of, 687 

bloodvessels of, 696 

fatty, 697 

-fluke disease, 211 

functions of, 687 

passive congestion of, 703 

pathological pathology of, 687 

red atrophy of, 703 

sarcoma of, 720 

syphilis of, 28, 186 

tropical, 702, 705 

tuberculosis of, 119 

tumors of, 719 



INDEX 



935 



Lobstein's cancer, 799 

Local infections, 63 

Lockjaw, 149 

Locomotor ataxia, 853 

Lorain type of infantilism, 335 

Lud wig's angina, 137, 597 

Lues, 180 

Lumbago, 911 

Lumbar myelitis, transverse, 880 

plexus, 824 
Lung, abscess of, 559 

compression of, 547 

fever, 71 

fibroid induration of, 552 

-fluke disease, 211 

gangrene of, 561 

pneumococcic infection of, 71 

sclerosis of, 552 

tumors of, 562 
Lungs, congestion of, 541 

diseases of, 539 

cedema of, 543 

hyperemia of, 541 

tuberculosis of, 108 
Lupinosis, 300 
Luschka's tonsil, 601 
Lymph nodes and lymph vessels, diseases 
of, 393 
tuberculosis of, 100 
Lymphadenitis, 393 
Lymphadenoma, 397 
Lymphangiectasis, 395 
Lymphangioma, 397 
Lymphangiosarcoma, 397 
Lymphangitis, 393 

Lymphatic system, tuberculosis of, 100 
Lymphatism, 403 
Lymphemia, 364, 378 
Lymphocytoma, 397 
Lymphocytosis, 364 
Lymphoma, 397 

malignant, 397 
Lymphomatosis, 397 
Lymphosarcoma, 397 
Lysins, 21 
Lyssa, 266 

M 

MICROGLOSSIA, 596 

Madura foot, 170 
Maidism, 300 
Main-en-griffe, 823 
Mai de caderas, 174 
Maladie de Woillez, 541 

du coit, 174 
Malarial cachexia, 209 

infections, 197 

latent and masked, 209 
Malignant pustule, 171 
Malleus humidus, 159 
Malta fever, 164 
Mania a potu, 290 
Marie's ataxia, 857 



Marsh fever, 197 
Mastigophora, 173 
Measles, 247 

German, 250 
Meat poisoning, 299 
Median nerve, 823 
Mediastinal tumor, 501 
Mediastinitis, 584 

Mediastinopericarditis, indurative, 750 
Mediastinum, diseases of, 584 

tumors of, 585 
Mediterranean fever, 164 
Medina-worm infection, 223 
Medulla, lesions of, 836 
Megalosplenic polycythemia or erythro- 

cythemia, 385 
Melanicterus, 692 
Membranous croup, 137 
Meniere's disease, 819 
Meningeal breathing, 509 

hemorrhage, 825 
Meningitis, cerebrospinal, 86 

external pachy-, 826 

internal pachy-, 827 

lepto-, 828 

purulent, 829 

serous, 829 

suppurative, 829 

syphilitic, 187 

tuberculous, 122 
Meningococcic infection, 86 
Meralgia paraesthetica, 810 
Mercurial poisoning, 297 
Mesenteric vessels, infarction of, 682 
Metabolic type of infantilism, 336 
Metabolism, disorders of, 303 
Metallic tinkle of Laennec, 582 
Metatarsalgia, 810 
Metazoan infections, 211 
Methylene blue test, 762 
Miasmatic diseases, 17 
Micromegaly, 336 
Migraine, 886 
Mikulicz's disease, 597 
Miliary fever, 274 
Milk poisoning, 299 

sickness, 274 
Millar's asthma, 404 
Miller's phthisis, 554 
Millstone-maker's phthisis, 554 
Mind deafness, 844 
Miner's anemia, 218 
Mitchell's, S. Weir, disease, 907 
Mitral insufficiency, 455 

stenosis, 459 
Moebius' sign in exophthalmic goitre, 343 
Mononeuritis, 811 
Mononuclear leukocytosis, 364 
Morbilli, 247 
Morbus coxae senilis, 920 

maculosus, 389 

neonatorum, 387 
Moro cutaneous reaction, 126 
Morphine habit, 292 



936 



INDEX 



Mor van's disease, 885 
Mosquito, plasmodium malarise in, 202 
Mosquitoes, varieties of, 198 
Motor aphasia, 842 

disorders of intestine, 647 
of stomach, 614 

neuron, diseases of lower, 848 
of upper, 845 

and lower, 852 

neurons, 802 
Mouth breathing, 601 

diseases of, 587 

dry, 596 

tuberculous ulceration of, 117 
Moynihan's appendix dyspepsia, 670 
Mucous colic, 654 
Muguet, 592 

Muller's muscle, paralysis of, 824 
Multiple progressive hyaloserositis, 

750 
Mumps, 260 
Muscles, diseases of, 911 
Muscular strain of heart, 427 
Musculospiral nerve, 823 
Musset's sign in aortic insufficiency, 

464 
Myalgia, 911 
Myasthenia gastrica, 616 

gravis, 851 
Myatonia, congenital, 916 
Mycetoma, 170 
Mycoprotein, 21 
Mycosis intestinalis, 161 

pulmonalis, 161 
Mycotic stomatitis, 592 
Myelemia, 364, 378 
Myelitis, 879 

acute ascending, 881 

chronic, 881 

compression, 882 

disseminated, 881 

transverse, 880 
Myelocytosis, 364 
Myeloma, multiple, 401, 767 
Myelopathic albumosuria, 401, 767 
Myiasis, 226 
Myocardial degeneration, 431 

weakness or insufficiency, 424 
Myocarditis, acute, 431 

chronic interstitial, 434 
Myocardium, congenital weakness of, 
424 

diseases of, 423 

fibroid degeneration of, 434 

tuberculosis of, 106 
Myoclonus, 914 
Myopathy, primary, 912 
Myositis, 912 
Myotonia, congenital, 915 
Mytilotoxism, 300 
Myxcedema of adults, 347 

postoperative, 348 
Myxedematous infantilism, or cretinism, 
336 



N 



Nagana, 174 
Nakra fever, 278 
Nasal catarrh, acute, 512 
chronic, 544 

diphtheria, 137 

mucous membrane, tuberculosis of, 
106 
Nasha fever, 278 

Nasopharyngeal obstruction, chronic, 601 
Neapolitan fever, 164 
Necrosis, fat, 739 
Nemathelminthiasis, 218 
Nephritis, 772 

acute diffuse, 773 

parenchymatous, 773 
suppurative, 779 

cardiovascular, changes in, 760 

chronic diffuse indurative, 783 
non-indurative, 780 

interstitial, 783 

parenchymatous, 780 
Nephrolithiasis, 794 
Nephrolysins, 21 
Nephroptosis, 685, 770 
Nerve, circumflex, 823 
Nerves, diseases of, 808 
Nervous belching, 615 

debility or disability, 895 

diarrhoea, 647 

diseases of functional or unknown 
nature, 886 

dyspepsia, 621 

exhaustion, 895 

prostration, 895 

system, diseases of, 811 

pathological physiology of, 
801 
tuberculosis of, 122 

vomiting, 615 
Neuralgia, 808 

cervicobrachial, 899 

cervicooccipital, 809 

intercostal, 809 

lumbar, 809 

paraesthetica, 824 

phrenic, 809 

plantar, 810 

red, 907 

trifacial, 808 

trigeminal, 808 
Neuralgias, visceral, 810 
Neurasthenia and psychasthenia, 895 
Neuritis, 811 

alcoholic, 812 

arsenical, 812 

diphtheritic, 812 

multiple, 275, 811 
Neurofibromatosis, generalized, 814 
Neuromas, 814 

amputation, 814 

plexiform, 814 
Neuromuscular disorders of heart, 415 



INDEX 



937 



Neurons, 801 

motor, 802 

sensory, 803 
Neuroretinitis, 815 
Neuroses, occupation, 897 

professional, 897 
Neurotic stomatitis, chronic, 591 
Newborn, hemorrhage in, 387 
Night blindness, 815 
Nigrities, 595 
Nocardiosis, 171 
Nodal rhythm, 419 
Noma, 593 

Non-bacterial fungus infections, 168 
Nose, diseases of, 511 

-bleeding, 511 
Nothnagel's vasomotor angina, 416 
Nurse's contracture, 350 
Nutmeg liver, 703 
Nyctalopia, 815 



Obesity, 327 

Obliterative pericarditis, 485 

peritonitis, 749 

pleuritis, 577 
Obstetrical or birth paralysis, 821 
Obstructive biliary cirrhosis, 732 
Ochronosis, 758 
Oculomotor nerve, 816 
(Edema, acute pulmonary, 543 

chronic pulmonary, 543 

of brain, 862 

of cardiac disease, 414 

of glottis, 519 

of larynx, 519 

of lungs, 543 

of tongue, 596 

pleural, 579 

recurrent pulmonary, 543 

suffocative pulmonary, 543 
(Edematous laryngitis, 519 
(Esophagismus, 606 
Oesophagitis, acute, 605 

chronic, 605 
(Esophagus, carcinoma of, 607 

diseases of, 605 

dilatation of, 606 

diverticula of, 606 

paralysis of, 607 

rupture of, 606 

spasm of, 606 

spasmodic stricture of, 606 

stenosis of, 607 

tuberculosis of, 117 

ulceration of, 605 

varices of, 606 
Oidiomycosis, 172 
Olfactory nerve, 814 
Oligopncea, 509 
Oliver's sign in aneurysm, 499 
Oliguria, 756 
Onomatomania, 903 



Oocyst, 174 
Ophthalmoplegia, 817, 851 

external, 852 

internal, 852 
Opium habit, 292 
Oppenheim's disease, 916 
Opsonins, 22 
Optic atrophy, 815 

chiasm, 815 

nerve, 815 

neuritis, 815 

tract and centre, 816 
Optical aphasia, 842 
Oriental sere. 196 
Orthopncea, 508 
Orthostatic albuminuria, 765 
Osteitis deformans, 922 
Osteo-arthritis, chronic hypertrophic, 920 
Osteogenesis imperfecta, 923 
Osteomalacia, 921 

of puberty, 329 
Oxyuriasis, 220 



Paget's disease, 922 
Pachymeningitis, external, 826 

internal, 827 
Painter's colic, 295 
Palpitation of heart, 416 
Palsy, bulbar, 850 

pseudobulbar, 851 

shaking, 898 
Paludism, 197 
Pancreas, cysts of, 743 

diseases of, 737 

hemorrhages into, 737 

tuberculosis of, 119 

tumors of, 744 
Pancreatic calculi, 745 

juice, 644 
Pancreatitis, acute, 738 

chronic, 741 

gangrenous, 738 

hemorrhagic, 738 

suppurative, 739 
Papillitis, 815 
Papillcedema, 815 
Paragonimiasis, 211 
Paralysis, acute ascending, 881 

agitans, 898 

bulbar, 850 

driver's, 878 

family periodical, 904 

glosso-labio-laryngeal and pharyn- 
geal, 850 

lead, 295 

of insane, 855 

of intestine, 648 

of oesophagus, 607 

unilateral ascending and descending, 
848 
Paramyoclonus multiplex, 914 



938 



INDEX 



Paranephritis, 792 
Paraphasia, 842 
Paraplegia, 846 

ataxic, 858 

spastic, 845 

hereditary, 847 
of adults, 845 
of infants, 846 
Parasites, malarial, 199 

estivo-autumnal, 201 
quartan, 200 
tertian, 199 

metazoan, 211 

protozoan, 173 
Parasitic insects, 225 

stomatitis, 592 
Parathyroid glands, diseases of, 349 
Paratyphoid fever, 60 
Parenchymatous and fatty degeneration 
of heart, 431 

hepatitis, 705 

nephritis, subacute and chronic, 780 

tonsillitis, 599 
Paresthesia of intestine, 650 
Parkinson's disease, 898 
Parorexia, 617 
Parosmia, 814 
Parotid bubo, 596 

gland, inflammation of, 596 
Parotitis, 596 

acute symptomatic, 596 

chronic, 597 

epidemic, 260 

infectious, 260 
Paroxysmal albuminuria, 765 

tachycardia, 422 
Parry's disease, 342 
Pathways of infection, 19 
Pediculosis, 225 
Pellagra, 300 
Pemphigoid purpura, 389 
Perforation in typhoid fever, 42 
Pericardial transudate, 487 
Pericarditic pseudocirrhosis of liver, 750 
Pericarditis, 748 

chronic, 484 

external, 485 

fibrinous, 478 

purulent, 483 

serofibrinous, 480 

suppurative, 483 

with effusion, 480 
Pericardium, adherent, 485 

air and gas in, 488 

blood in, 487 

diseases of, 478 

dropsy of, 487 

empyema of, 483 

tuberculosis of, 103 
Pericholecystic adhesion, chronic, 733 
Perichondritis, laryngeal, 522 
Perihepatitis, 704 
Perinephritic abscess, 792 
Perinephritis, 792 



Peripheral facial paralysis, 818 
Perisigmoiditis, 672 
Peritoneum, diseases of, 746 

tuberculosis of, 103 
Peritonitis, acute, 748 

chronic, 749 

hyperplastic, 750 

deforming, 750 

hyaline, 750 
Pernicious anemia, 373 

estivo-autumnal malarial infection, 
207 
algid form, 208 
comatose form, 207 
hemorrhagic form, 208 
Peroneal type of progressive muscular 

atrophy, 849 
Perpetual irregularity, 419 
Pertussis, 257 
Perverted appetite, 617 » 
Pestis ambulans, 158 

minor, 158 
Petruschky's spinalgia, 101 
Pfeiffer phenomenon, 21 
Phagedena, tropical, 282 
Pharyngeal tonsil, 601 

diphtheria, 136 
Pharyngitis, 598, 603 

acute, 603 

chronic, 603 
Pharyngocele, 606 

Pharynx, acute infectious phlegmon of, 
604 

diseases of, 598 

tuberculosis of, 117 

ulceration of, 603 
Phlebectasis, hemorrhoidal, 683 
Phlebitis, hepatic, 696 
Phlegmonous enteritis, 667 

laryngitis, 519 

tonsillitis, 599 
Phloridzin test, 762 
Phthiriasis, 225 
Phthisis, 92 

fibroid, 552 

miller's, 554 

ventriculi, 627 
Piles, 683 

Pinworm infection, 220 
Piroplasmosis, 195 

von Pirquet's cutaneous reaction, 125 
Pituitary body, diseases of, 355 

tumors of, 836 
Plague, 156 
Plasmodium kochi, 174 

malarise in man, 199 
in mosquito, 202 
Plethora and polycythemia, 363 
Pleura, diseases of, 564 

tuberculosis of, 102 

tumors of, 584 
Pleural dropsy, 579 

oedema, 579 
Pleurisy, 564 



INDEX 



939 



Pleurisy, chronic adhesive, 577 

diaphragmatic, 570 

dry, plastic, or acute adhesive, 564 

interlobar, 571 

suppurative, 574 

with effusion, 566 
chronic, 577 
Pleuritis, 564 

Baccelli's sign in, 569, 575 

chronic, 577 

fibrinous, 564 

Grocco's sign in, 569 

hemorrhagic, 576 

purulent, 574 

serofibrinous, 566 
Pleurodynia, 911 
Pleuropericarditis, 485 
Plumbism, 294 
Pneumothorax, 580 
Polyorrhomenitis, 578 
Pneumaturia, 758 
Pneumococcic infection, 70 
of lungs, 24, 71 

septicemia, 70 
Pneumogastric or vagus nerve, 819 
Pneumonokoniosis, 554 
Pneumonia, 71 

alcoholic, 79 

apical, 79 

asthenic or adynamic, 79 

basal, 79 

bilious or malarial, 80 

central, 79 

clinical varieties of, 79 

complications and sequels of, 81 

croupous, 24 

diagnosis of, 82 

double, 79 

epidemic, 79 

ether, 80 

etiology of, 71 

. fever in, 75 

in aged, 80 

in children and infants, 80 

larval or abortive, 79 

latent, 79 

lobular, 549 

massive, 79 

migratory or creeping, 79 

pathology of, 72 

physical signs of, 77 

postoperative, 80 

prognosis of, 82 

secondary, 80 

symptoms of, 73 

temperature in, 74 

terminal, 80 

toxic, 80 

treatment of, 82 

typhoid, 79 
Pneumonic plague, 158 

tuberculosis, acute, 109, 115 
Pneumonitis, 71 
Pneumopericardium, 488 



Pneumothorax, 582 

Podagra, 320 

Polioencephalitis, inferior, 850, 871 

superior, 851,871 
Poliomyelitis, acute, 270 

chronic anterior, 841 

epidemic, 270 
Polyarthritis, chronic, atrophic tvpe of 

Goldthwait, 918 
Polycythemia, 363 

with cyanosis and enlarged spleen, 385 
Polynuclear leukocytosis, 364 
Polyorrhomenitis, 105, 750 
Polyphagia, 617 
Polypnoea, 508 
Polyserositis, 750 
Polyuria, 318,756 
Ponos, 279 
Pons, lesions of, 836 
Portal vein, 696 
Postural albuminuria. 765 
Potter's rot or asthma, 554 
Preacher's sore throat, 521 
Precipitins, 21 
Proctitis, gangrenous, 281 
Prof eta's law, 181 
Proteosoma, 174 
Protozoa, 173 

Protozoan infections, 27, 173 
Protozoic dermatitis, 172 
Progressive muscular atrophy, 852 

of Charcot-Marie-tooth 

type, 849 
of Duchenne-Aran type, 848 
of Yulpian type, 848 
peroneal tvpe. 849 
dystrophy, 912 

neural muscular atrophy, 849 

spinal muscular atrophy, 848 
Pseudohvpertrophic muscular paralysis, 

912 
Pseudoleukemia, 397 
Pseudomembranous enteritis, 654 
Pseudotuberculosis, 171 
Psilosis, 281 
Psittacosis, 287 
Psoriasis of tongue, 595 
Psorospermiasis, 172 
Psychical blindness, 844 

deafness, 844 
Ptomaine poisoning, 299 
Ptyalism, 591, 596 
Pulmonary apoplexy, 545 

aspergillosis, 171 

congestion, 541 

embolism and thrombosis, 545 

hemorrhage, 539 

infarction, 545 

insufficiency, 470 

oedema, 543 

stenosis, 470 
Pulse, alternating, 421 
Purpura, 387 

abdominal, 389 



940 



INDEX 



Purpura fulminans, 390 

hemorrhagic, 389 

Henoch's, 388, 389 

idiopathic, 388 

rheumatica, 389 

symptomatic, 388 
Putrid bronchitis, 528 
Pyelitis, 788 
Pyemia, 61 
Pyelonephritis, 788 
Pyelonephrosis, 788 
Pylephlebitis adhesiva, 696 

suppurative, 697 
Pylethrombosis, 696 

Pylorus, insufficiency or incontinence of, 
616 

spasm of, 615 
Pyococcic infection, 61 
Pyogenic infections, 61 
Pyopneumopericardium, 488 
Pyopneumothorax, 580 

subphrenic, 749 
Pyuria, 769 



Q 



QUADRIGEMINAL pulse, 418 

Quartan malarial infection, 203, 205 

parasite, 200 
Quincke, penetrating or centripetal pulse 
of, 465 
serous meningitis of, 829 
Quincke's disease, 907 
Quinquageminal pulse, 418 
Quinsy, 599 

Quotidian estivo-autumnal malarial infec- 
tion, 206 



Rabies, 266 
Rachitic rosary, 330 
Rachitis, 329 

tarda, 329 
Rag-picker's disease, 161 
Railway brain, 896 

spine, 896 
Ranula, 596 
Raynaud's disease, 908 
von Recklinghausen's disease, 814 
Recurrent pulmonary oedema, 543 
Reichmann's disease, 619 
Reflexes, 805 

Relapses in typhoid fever, 48 
Relapsing fever, 178, 224 
Renal calculus, 794 

disease, hypertrophy of heart in, 439 

tuberculosis, 121 
Respiratory system, diseases of, 505 

tuberculosis of, 106 
Retropharyngeal abscess, 604 
Rheumatic fever, 253 
Rheumatism, acute and subacute, 253 

articular, 253 



Rheumatism, muscular, 911 
Rheumatoid arthritis, 918 
Rhinitis, acute, 512 

chronic, 544 

fibrinous, 137 
Rhizopoda, 173 
Rhythm of auricular paralysis, 419 

• nodal, 418, 419 
Remittent fever, 197 
Rickets, 329 

acute, 330, 333 
Riedel's lobe, 695 
Riga's aphtha, 591 

disease, 591 
Ringworm of tongue, 595 
Rock fever, 164 

Rocky Mountain spotted fever, 224, 269 
Rosenbach, erysipeloid of, 69 
Rosenbach's sign in exophthalmic goitre, 

343 
Rose, cephalic tetanus of, 151 

cold, 515 
Roseola, epidemic, 250 
Rotch's sign in pericarditis, 481 
Rotheln, 250 

Roundworm infection, 218 
Rubella, 250 

notha, 250 
Rubeola, 247 
Rupture of heart, 444 

of oesophagus, 606 

of spleen, 406 



S 



Sacra.l plexus, 824 
Salivary calculi, 597 

glands, diseases of, 596 
hypersecretion of, 596 
Saltatory spasm, 904 
Sand, intestinal, 683 
Sapremia, 61 
Sarcodina, 173 
Sarcoma, 349, 798 
of larynx, 523 
of liver, 720 
Sarcoptic itch, 224 
Scarlet fever, 240 

complications and sequels of, 244 
diagnosis of, 244 
etiology of, 240 
pathology of, 241 
prognosis of, 245 
symptoms of, 241 
treatment of, 245 
varieties of, 243 
Schmidt's test diet, 652 
Schonlein's disease, 389 
Sciatica, 809 

Sclerosis, disseminated, 859 
insular, 859 
multiple, 859 
of coronary arteries, 434 



INDEX 



941 



Sclerosis of lung, 552 

of spinal cord, subacute combined, 
858 

posterior, 853 

posterolateral, 858 

toxic combined, 858 

ventriculi, 627 
Scorbutus, 331 
Screw-worm, 226 
Scrofula, 92 
Scurvy, 331 

infantile, 333 

-rickets, 333 
Seatworm infection, 220 
Secondary infection, 64 
Secretory disorders of intestine, 650 

of stomach, 618 
Senile tremor, 900 
Sensory disorders of intestine, 649 
of stomach, 616 

neuron, 803 

diseases of, 853 
Septic infections, 61 
Septicemia, 61, 64 
Septicemic plague, 158 
Septicopyemia, 61 

Septicopyemic abscesses, multiple, 708 
Serofibrinopneumothorax, 580 
Serositis, multiple, 105, 578, 750 
Serous membranes, tuberculosis of, 102 
Seven-day fever, 178 
Ship fever, 237 
Siberian liver-fluke disease, 212 

opisthorchiasis, 212 
Siderosis, 554 
Sighing in diseases of respirator}' - system, 

510 
Sigmoid diverticulitis, 672 
Sinus irregularity, 416 
Siriasis, 905 
Sitotoxism, 300 
Sleeping sickness, 194 
Smallpox, 226 

complications of, 231 

diagnosis of, 231 

prognosis of, 232 

treatment of, 232 

varieties of, 230 
Smith's sign in tuberculosis of lymph 

nodes, 101 
Smoker's tongue, 595 
Snake- venom poisoning, 298 
Sneezing in diseases of respiratory sys- 
tem, 510 
Snuffles, 188 

Sobbing in diseases of respiratory sys- 
tem, 510 
Soldier's heart, 427 
Somatic teniasis, 217 
Soor, 592 
Sore throat, 598 

clergymen's, 603 
preacher's, 521 
Sparganum mansoni, 2 IS 



Sparganum proliferum, 218 
Spasm habit, 901 

of cardia, 615 

of intestine, 648 

of oesophagus, 606 

of pylorus, 615 
Spastic cerebral paraplegia, 846 

diplegia, 846 

paralysis of infants, 846 

paraplegia, 845 

hereditary, 847 

spinal paralysis, 845 

tabes, 845 
Spinal accessory nerve, 820 

cord, 837-840 

anemic degeneration of, 858 
compression of, 882 
diffuse and focal diseases of, 876 
hemorrhage into, 876 
secondary degeneration of, 858 
subtotal transverse lesion of, 837 
total transverse lesion of, 837 
tumors of, 883 
unilateral lesions of, 838 

gliosis, 884 

meningeal hemorrhage, 826 

nerves, diseases of, 821 
Spirillosis, 178 
Spirochsetse, 173 
Spirochetosis, 178 
Splanchnoptosis, 685 
Spleen, diseases of, 405 

enlargement of, 407 

floating, 406 

movable, 406 

rupture of, 406 

tuberculosis of, 102 
Splenic anemia, 407, 408 

fever, 161 

pseudoleukemia, 400 

tumor, acute, 407 
chronic, 407 
Splenomegaly, 407 

Gaucher type of, 408 

tropical, 195 
Splenoptosis, 406, 685 
Spondylose rhizomelique, 921 
Sporozoa, 174 
Spotted fever, 86, 237 
Sprue, 281 

S-shaped curve of Ellis and Garland, 568 
St. Anthony's fire, 67 
St. Vitus' dance, 900 
Staphylolysin, 21 
Status epilepticus, 890 

lymphaticus, 403 
Steatorrhcea, 737 

Stellwag's sign in exophthalmic goitre, 343 
Stenocardia, 493 
Stenosis, 607 

aortic, 466 

mitral, 459 

of intestine, 674 

of oesophagus, 607 



942 



INDEX 



Stenosis of pylorus, 630, 643 

pulmonary, 470 

tricuspid, 469 
Stokes, bellows murmur of, 465 
Stomach, acute dilatation of, 629 

atony of, 616 

carcinoma of, 638 

chronic dilatation of, 630 

diseases of, 608 

loss or impairment of appetite 

in, 610 
nausea and vomiting in, 612 
thirst in, 611 

excessive amount of gases in, 611 

hemorrhage from, 613 

hyperesthesia of, 616 

motor disorders of, 614 

non-carcinomatous tumors of, 643 

peristaltic unrest of, 615 

secretory disorders of, 618 

sensory disorders of, 616 

symptomatic disorders of, 610 

tuberculosis of, 117 

ulcer of, 632 
Stomatitis, 587 

aphthous, 589 

catarrhal, 589 

croupous, 591 

epidemic, 273 

gangrenous, 593 

infectious, 587 

mechanical, 588 

membranous, 591 

mercurial, 591 

thermic, 588 

toxic, 588 

ulcerative, 590 
Stonecutter's phthisis, 554 
Streptolysin, 21 
Streptothricosis, 171 
Stricture of oesophagus, 606 
Stridulus laryngitis, 520 
Stroke, 862 
Strongyloidosis, 219 
Struma, 340 
Subinfection, 25 
Succus entericus, 645 
Sudoral typhoid, 40 
Suffocation, 510 

Summer diarrhoea of children, 661 
Sunstroke, 905 
Superacidity, 618 
Surra, 174 
Swamp fever, 197 
Sweating sickness, 274 
Sydenham's chorea, 900 
Syncope, local, 908 
Synovitis, gonococcic, 91 
Syphilis, 180 

acquired, 180 

bones, joints, bursse, and muscles in, 
_ 187 

circulatory system in, 185 

congenital, 181 



Syphilis, cutaneous lesions of, 186 

diagnosis of, 189 

digestive system in, 186 

etiology of, 180 

general symptoms of, 183 

genito-urinary system in, 186 

mucous membrane lesions of, 184 

nervous system in, 187 

of liver, 186 

pathology of, 181 

prognosis of, 189 

respiratory system in, 185 

treatment of, 190 
Syphilitic bursopathy of Verneuil, 188 

liver, 28 
Syringomyelia, 884 



Tabardillo, 237 
Tabes dorsalis, 853 

arthropathies in, 855 
etiology of, 853 
pathology of, 853 
symptoms of, 854 
treatment of, 856 
Tabo-paralysis, 855 
Tachycardia, 421 

paroxysmal, 418, 422 
Tachypncea, 508 
Taenia echinococcus, 217 
mediocanellata, 214 
saginata, 214 
solium, 215 
Tapeworm, beef, 214 
dwarf, 216 
fish, 215 
infection, 214 
pork-measly, 215 
Tay-Sachs disease, 847 
Telangiectasis of skin and mucous mem- 
brane, multiple, 511 
Tellais' sign in exophthalmic goitre, 344 
Teniasis, 214 

diagnosis of, 216 
intestinal, 214 
somatic, 217 
symptoms of, 216 
treatment of, 216 
Terminal or secondary infections, 64 
Tertian estivo-autumnal malarial infec- 
tion, 205 
malarial infection, 203 
parasite, 199 
Tetanolysin, 21 
Tetanus, 149 

hydrophobicus, 151 
idiopathic, 149 
traumatic, 149 
Tetany, 350 
Texas fever, 224 
Thalamus, lesions of, 836 
Thermic fever, 905 



INDEX 



943 



Thirst in diseases of stomach, 611 
Thomsen's disease, 915 
Thoracic duct, disease of, 401 

myelitis, transverse, 880 

nerve, long or posterior, 823 
Threadworm infection, 220 
Thrombosis of cavernous sinus, 870 

of cerebral sinuses, 870 

of kidney, 771 

of lateral sinus, 870 

of longitudinal sinus, 870 

of lung, 545 

of mesenteric veins, 682 

of spleen, 406 
Thrush, 592 

Thymic tracheostenosis, 403 
Thymus body, diseases of, 402 

enlargement of, 403 
Thyroid, diseases of, 339 
Thyroiditis, acute, 340 
Thyroids, aberrant or accessorv, 349 
Tic convulsif, 903 

impulsive, 903 
habit, 901 

douloureux, 808 
Tick fever, 224, 269 

infection, 224 
Tongue, acute oedema of, 596 

black, 595 

diseases of, 594 

eczema of, 595 

geographical, 595 

ichthyosis of, 595 

leukoplakia of, 595 

psoriasis of, 595 

ringworm of, 595 

smoker's, 595 

tylosis of, 595 

wandering rash of, 595 
Tonsil, Ungual, 604 

Luschka's, 601 

pharyngeal, 601 
Tonsillar abscess, 599 
Tonsillitis, 598 

acute, 598 

chronic, 601 
Tonsils, diseases of, 598 

enlarged, 601 

hypertrophied, 601 

tuberculosis of, 117 
Torticollis, 820, 912 
Toxemia, 22, 61 
Toxins and antibodies, 20 

extracellular, 20 

intracellular, 21 
Trachea and bronchi, diseases of, 524 

tuberculous ulceration of, 108 
Tracheal and bronchial obstruction, 537 
Tracheitis, acute, 524 
Tracheobronchitis, acute, 524 
Traumatic neuroses and psychoses, 896 
Transcortical aphasia, 842 
Transmission of infectious diseases, 18 
Traube's sign in aortic insufficiency, 464 



Trematode infections, 211 
Trembles, 274 
Treponema^, 173 
Trichuriasis, 221 
Trichinosis, 221 
Trichocephaliasis, 221 
Trichomonas, 174 
Tricuspid insufficiency, 468 

stenosis, 469 
Trigeminal nerve, 817 

pulse, 418 
Trismus neonatorum, 150 
Trochlear nerve, 816 
Tropical abscess of liver, 708 

phagedena, 282 
Trousseau's sign in tetany, 351 
Trypanosoma?, 174 
Trypanosomiasis, 194 
Tsetse-fly disease, 194 
Tubercula dolorosa, 814 
Tuberculin in treatment of tuberculosis, 
129 

tests, 125 
Tuberculosis, 92 

acute miliary, 96 
pneumonic, 109 

bloodvessels in, 106 

chronic fibroid, 110 
ulcerative, 109 

etiology of, 92 

fresh air, nutritious food, rest, and 
exercise in, 127 

general diagnosis of, 125 

laryngeal, 107 

medicinal treatment of, 130 

miliary, 102 

of bones and joints, 124 

of cerebral meninges, 122 

of circulatory system, 106 

of digestive system, 117 

of female genitalia, 120 

of genito-urinary system, 120 

of intestines, 118 

of liver, 119 

of lungs, 108 

classification of, 116 
diagnosis of, 115 
pathology of, 109 
prognosis of, 115 
symptoms of, 110 

of lymph nodes, 102 

of lymphatic system, 100 

of meninges, 829 

of myocardium, 106 

of nasal mucous membrane, 106 

of nervous system, 122 

of oesophagus, 117 

of pancreas, 119 

of pericardium, 103 

of peritoneum, 103 

of pharynx, 117 

of pleura, 102 

of respiratory system, 106 

of serous membranes, 102 



944 



INDEX 



Tuberculosis of several serous mem- 
branes, 105 
of stomach, 117 
of testicle, 120 
of tonsils, 117 
of urinary system, 121 
pathology of, 94 
peritoneal, 104 

prophylactic measures in, 126 
pulmonary, 108 

special forms of, treatment of, 131 
specific remedies in treatment of, 129 
surgical intervention in, 131 
treatment of, 127 
tuberculin in treatment of, 129 
Tubular diarrhoea, 654 
TufnelPs treatment in aneurysm, 502 
Tumors and tumor-like formations of 
lymph nodes, 397 
of bladder, 799 
of brain, 873 
of heart, 444 
of intestine, 676 
of kidney, 798 
of larynx, 523 
of liver, 719 
of lungs, 562 
of mediastinum, 585 
of pancreas, 744 
of pleura, 584 
of spleen, 410 
of thyroid, 349 
Tunica vaginalis, chylous dropsy of, 223 
Tylosis of tongue, 595 
Typhoid carriers, 34, 37 
cholera, 154 
fever, 32 

characteristic lesions of, 36 

chills in, 40 

circulatory system in, 44 

color of skin in, 40 

diagnosis of, 49 

diarrhoea in, 41 

diet in, 52 

digestive system in, 41 

epistaxis in early stages of, 43 

eruptions in, 40 

etiology of, 33 

general management of, 51 

genito-urinary system in, 46 

hemorrhage in, 59 

hydrotherapy in treatment of, 
53 

intestinal hemorrhage in, 42 

leukopenia in, 44 

liver in, 43 

nervous system in, 45 

pathology of, 34 

perforation in, 42, 59 

peritonitis in, 43 

prognosis of, 50 

recurrence in, 49 

relapses in, 48 

respiratory system in, 43 



Typhoid fever, symptoms of, 37 
temperature in, 38 
treatment of, 50 
tympanites in, 41 
varieties of, 47 
pneumonia, 79 
pneumonitis, 34 
sudoral, 40 
Typhus fever, 237 

of Mexico, 237 
Tyrotoxism, 299 



Ulcer of stomach and duodenum, 632 
etiology of, 432 
pathology of, 633 
symptoms of, 634 
treatment of, 636 
of intestine, 673 
of oesophagus, 605 
of pharynx, 603 
tropical, 196 
Ulcerating granuloma of genitals, 283 
Ulcerative tuberculosis, chronic, 109, 115 
Ulnar nerve, 823 
Uncinariasis, 218 
Undulant fever, 164 
Uremia, 759 
Ureteritis, 788 
Urethra, tuberculosis of, 14 
Urinary system, diseases of, 755 

tuberculosis of, 121 
Urine, abnormal constituents in, 757 
abnormally colored, 758 
electrical conductivity of, 763 
variations in normal constituents of, 
756 
Uvula, elongation of, 604 



Vaccination, method of, 233 

Vaccines, bacterial, 32 

Vaccinia, 233 

Valvular disease of heart, chronic, 452 
diagnosis of, 472 
prognosis of, 472 
treatment of, 473 
lesions, combined, 471 

Vaquez's disease, 385 

Varicella, 235 

Varices, 606 

Varicose axillary glands, 223 
groin glands, 223 

Variola, 226 

Vasomotor and trophic disorders, 907 

Varix, cutaneous and deep lymphatic, 
223 

Vegetable poisoning, 301 

Venal distomatosis, 213 

Ventricle, hypertrophy and dilatation of 
left, 442 



INDEX 



945 



Ventricle, hypertrophy and dilatation of, 

right, 442 
Ventricular extrasystoles, 417 

rhythm, 419 
Verneuil, syphilitic bursopathy of, 188 
Verruga, 284 
Vertigo, paralytica, 285 
Vestibular nerve, 819 
Vincent's angina, 139 
Virchow's giant growth of colon, 682 

smooth atrophy of base of tongue, 185 
Visceroptosis, 685 
Vitiligoidea, 693 
Volkmann's contracture, 823 
Vomiting, cyclic or periodic, 615 

nervous, 615 

primary periodic, 615 



W 



Wassermann complement-binding test, 
28 
deviation-of-the-complement test,28 
reaction in syphilis, 189 
Waxy or bacony degeneration, 334 
Weil's disease, 272, 691 
Wernicke's hemiopic pupillary reaction, 

816 
Whipworm infection, 221 
White patches or milk spots on pericar- 
dium, 484 
Whooping cough, 257 
Winckel's disease, 387 
Winter cough, 527 

chronic, 528 



Wintrich's sign in tuberculosis of lungs, 

114 
Wolff-Eisner conjunctival test, 126 
Wooden tongue, 169 
Wool-sorter's disease, 161 
Word-blindness, 841 
Word-deafness, 841 
Wound diphtheria, 138 
Wrist-drop, 812 
Writer's cramp, 897 
Wry-neck, 912 



X-rays, use of, in pneumonia, 86 
Xanthelasma, 693 
Xanthoma, 693 
Xerostomia, 596 



Yawning in diseases of respiratory sys- 
tem, 510 
Yaws, 193 
Yellow fever, 261 



Zenker's degeneration in typhoid fever, 

36 
Zooparasites, 20 
Zooparasite infections, 173 
Zuckergussleber, 578, 750 
Zuckergusslunge, 750 
Zuckergussmilz, 750 
Zuckerkandl's bodies, 351 



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